CPG Version 1 - 4 2019-1

Ambulance Service
Clinical Practice Guidelines
CPG Ver. 1.4. - 2019

VERSION CONTROL PAGE
VERSION HISTORY
Document Document Revision Project Authors Date
Versions* History / Reviewer / Reviser
[insert version [Briefly describe work completed [Name author or reviser] [insert version
number] to create the version] completion date]
1.0 Initial Draft Mr. Casey Walker 2016
1.1 Addendum CW, JPS 20170509
1.1 final addendum and corrections CW, JPS 20170805
1.2 version no. updated JPS 20170809
1.3 Quarterly update (changes IRH, YP, ILH, BDL, NC 20180517

made)
1.4 Quarterly update (changes IRH, YP, ILH, BDL, NC 2019
made)
APPROVALS
Date Document Version Approver Name and Title Approver
Signature
[insert approv- [Insert version approved] [Provide name and title/ role of approver] [Provide signature]
al date]
Dr. Loua Al Sheik, Medical Director
Dr. Robert Owen, CEO HMCAS
Mr. Brendon Morris, Executive Director

HMCAS
Dr. Nicholas Castle, Head of Profession
Dr. Padarath Gangaram, A/SOM:

Training
Message from Her Excellency
An excellent ambulance service saves lives. In Qatar, a strong first response service is particularly important be-
cause of the high rates of workplace and traffic accidents that we face, among many other urgent and emergency
episodes.
Here at Hamad Medical Corporation we are proud to have a fast and high quality Ambulance Service that is
reaching and caring for acutely ill patients at their time of greatest need.
It is a testament to the strong leadership of the service and the dedication and professionalism of its staff that our
Ambulance Service is the first of its type in the region to receive Joint Commission International accreditation.
However, the Ambulance Service, like all of our services, will not rest on its laurels; it is on a quest for continual
improvement.
These new clinical guidelines for the Ambulance Service are an important part of that journey of improvement.
They will help to ensure that our critically ill patients receive the right care, as quickly as possible and are stabi-
lized or treated to give them the best chance of recovery.
There are a number of features of these new guidelines that I welcome in particular. They are the product of a
thorough and collaborative consultation with key stakeholders across the professional disciplines.
They are based on full pathways of care, so that they concentrate on the patient rather than a narrow part of the
acute healthcare system. They are also based on a robust evidence base, drawn from international best prac-
tice, and will be supported by a comprehensive program of education, so we can be confident in their implemen-
tation and efficacy.
I am very grateful to Dr Loua Al Shaikh, Medical Director, and Dr Robert Owen, Chief Executive Officer, for the
their excellent leadership of the Ambulance Service overall and the production of these new clinical guidelines
specifically. I am also very grateful to all members of staff of the Ambulance Service for the dedicated work they
are doing day-in and day-out for our patients.
With new clinical guidelines and new vehicles coming on stream, I have every confidence that our Ambulance
Service will continue to go from strength to strength in the future.
H.E. Hanan Al-Kuwari PhD

Minister of Public Health
Qatar
Message from the Medical Director
Over the past three years, and since publishing the last version of the HMC Ambulance Service
(HMC AS) clinical practice guidelines, much has happened to the service. In order to respond to
rising clinical need within the State of Qatar, the service has grown in size and has diversified into
specialized spheres of operations. In order to maintain the appropriate response to calls, by either
the public or the various medical facilities, the service now has more hubs, spokes and clinical units
to accommodate the widest spectrum of clinical need.
HMC AS’ clinical staff is the greatest asset the service has, therefore maintaining HMC AS clini-
cians’ professional standing through appropriate guidance, training and education is of the highest
importance. To that end, this latest version of HMC AS’ clinical practice guidelines has been devel-
oped to support that theme. These guidelines are based on the latest evidence and best practice in
the pre-hospital field. They have been updated through review of the latest published evidence and
the learning from the HMC AS’ clinical frontline.
The review and re-write process has taken a year to accomplish. I have to thank Mr. Craig Campbell
for leading this process and the many staff, too many to mention, representing all clinical levels of
the service, who contributed to the review and rewrite of these guidelines.
Finally, HMC AS clinicians should view these guidelines as clinical intervention recommendations to
help with their clinical decision-making.
Dr. Loua Asad Hanna Al Shaikh

Medical Director
HMC Ambulance Service
Dear Colleagues:
The purpose of these HMCAS Clinical Practice Guidelines are to:
 Provide a common clinical practice framework for Ambulance Practitioners from different healthcare systems
 Ensure consistent application of evidence and expert opinion-based clinical management.
 Provide guidance to facilitate decision making for infrequently encountered or complex clinical conditions.
 Facilitate a defence against alleged malpractice.
The Guidelines reflect a practical approach and where appropriate, link in with receiving hospital treatment path-
ways. The CPGs cannot cover all eventualities encountered within the complex and dynamic environment of
pre-hospital care. Safety – Benefit – Effectiveness trade-offs have to be made on a daily basis. At times, clinicians
will have to undertake care for conditions not covered, or use available tools and techniques for situations beyond
the published guidelines.
The guiding principle for those situations is to provide safe and effective patient care by concentrating on core
patient outcomes:
 Saving and preserving of life

 Relieving suffering
 Facilitate safe transfer to a specialist centre or hospital
 Maximising recovery from critical injury or illness
By moving away from paper-based editions HMCAS guidelines will now be reviewed more regularly taking account
changing national and international guidelines, feedback from Ambulance Practitioners of all grades as well as hos-
pital based colleagues. Best Practice Guidelines are an essential aspect of effective clinical governance and these
Clinical Practice Guidelines form the corner stone of clinical audit, pathway review and pathway development. For
the Ambulance Service to learn feedback from clinical practice is required. Clinicians have a professional respon-
sibility to highlight deviations and situations not covered by the CPGs to the medical directorate for the organisation
to review its practice and adapt.
Ambulance Paramedics remain the backbone of the ambulance service, providing care in all patient contacts. The
Clinical Guidelines address the vast majority of patient contacts, where a prehospital interventions are required to
be performed by an ambulance paramedic. Should a deviation from the clinical Guidelines be required, wherever
possible, the attending Ambulance Paramedic should discuss the patient’s needs with the Clinical Team Leader
based within the National Command Centre.
Critical Care Paramedics target a smaller number of patients who may require more advanced interventions. They
will face clinical situations that cannot be predicted and may have to, on occasions, act outside of these published
guidelines to manage a patient according to the principles mentioned above.
The wealth of experience, within our staff, remains essential to optimising patient outcomes and therefore our clini-
cal guidelines outline variations in clinical practice between Ambulance Paramedics and Critical Care Paramedics.
Dr. Nicholas Castle

Head of Profession: Ambulance Service
Specific Clinical Privileges
STAFF CIRCULAR HMCAS REF. NO. AS/SC 17-27
In addition to established procedures as per HMCAS Clinical Guidelines, Critical Care and Ambulance Paramedics
are privileged to autonomously carry out the clinical activities below subject to having undertaken in-service training
and being deemed competent (signed-off by the Associate Medical Director: Transfer and Retrieval Services) or
following an individual command decision by the on-call Transfer and Retrieval Consultant or Silver Clinical (if the
prior is unavailable).
PROCEDURE AP CCP COMMENTS

Care, Maintenance and Management of
Assist Carry out
Chest Tubes
Any ventilator in Service
Use of Ventilators Assist Carry out
use
Use of invasive and non-invasive venti-
Assist Carry out
lation modes
Adjustment of ventilator settings to
implement lung protective ventilation Silver Clinical discus-
Assist Carry out
or action on blood gases to achieve sion required
acceptable parameters.
Care, use, maintenance and manage-
Assist Carry out
ment of central lines
Care, use, maintenance and manage-
Assist Carry out
ment of arterial lines
Management of ECMO patients as
Assist Carry out
directed by Medical Staff
Care, Maintenance and Management of
Assist Carry out
indwelling urinary catheters
Silver Clinical discus-
Insertion of indwelling urinary catheters Carry out Assist
sion required
Use of point of care diagnostic devices
for blood gas, electrolytes and hemo-
Assist Carry out
globin, basic interpretation and action-
ing on results
Basic and advanced nursing care (eg.
Trach care, eye and mouth care, pres- Assist Carry out
sure care)
Level 3 patients under
indirect medical super-
vision at the discretion
Transport of Level 2 and 3 patients Carry out Carry out
of Silver clinical or
on-call Transfer and Re-
trieval ICU consultant
continuation of drug therapy, within
Assist Carry out
service specific formulary
Silver Clinical or on-call
continuation of drug therapy, outside
Transfer and Retrieval
service specific formulary where pre- Assist Carry out
ICU consultant discus-
scribed at the referral hospital
sion required
PROCEDURE AP CCP COMMENTS
Use of syringe and IV drivers Assist Carry out
Initiation, on independent assessment
of patient, of drug therapy within ser- Assist Carry out
vice specific formulary
Assessment of in-hospital level 2 and 3 Silver Clinical or on-call
patients for transfer and basic physio- Transfer and Retrieval
Assist Carry out
logical manipulation to improve clinical ICU consultant discus-
stability before and during transport sion required
Assessment using ultrasound Assist Carry out
Basic interpretation of radiological
investigations for the purpose of veri-
Assist Carry out
fying the correct position of indwelling
medical devices.
CONTENTS
click on the title to go to that page
ADULT MEDICAL GUIDELINES

CPG 1 Clinical Approach to an Adult Medical Patient 1
CPG 1.1 Conscious Status Assessment 8
CPG 1.2 Airway and Respiratory Status Assessment 9
CPG 1.3 Perfusion Status Assessment 12
CPG 2.1 Adult Foreign Body Airway Obstruction 15
CPG 2.2 Management of Upper Airway Swelling in Adults 19
CPG 2.2.1 Management of Anaphylaxis in Adults 22
CPG 2.3 Management of the Airway: Rapid Sequence Induction for Adults 25
CPG 3.1 Management of Adult Acute Bronchoconstriction

(including asthma, COPD and allergic reactions) 38
CPG 3.2 Management of Severe Respiratory Infection in Adult Patient 40
CPG 3.3 Oxygen Therapy 42
CPG 3.4 Mechanical Ventilation 45
CPG 4.1 Adult Medical Cardiac Arrest Management 53

CPG 4.2 Management of Acute Coronary Syndromes 57
CPG 4.3 Management of Acute Pulmonary Oedema 61
CPG 4.4 Management of Adult Sepsis 64
CPG 4.5.1 Management of Adult Symptomatic Bradyarrhythmias 66
CPG 4.5.2 Management of Adult Symptomatic Tachyarrhythmias 69
CPG 4.6 Management of Pulmonary Embolism 72
CPG 4.7 Management of Non-Traumatic Shock 73
CPG 5.1 Management of Stroke 77

CPG 5.2 Management of Adult Seizures 81
CPG 6.1 Management of Pain 83

CPG 6.2 Management of Nausea and Vomiting 87
CPG 6.3 Safe Sedation and Monitoring in Adults 89
CPG 7 Management of Hyperglycaemia and Hypoglycaemia 93
CPG 8 Management of Drug Overdose and Poisoning 94

CONTENTS
ADULT TRAUMA GUIDELINES

CPG 9 Clinical Approach to the Adult Trauma Patient 97
CPG 9.1 Adult Trauma Peri-arrest/ Cardiac Arrest Management 105
CPG 9.2 Management of Significant Haemorrhage and Haemorrhagic Shock 110
CPG 9.3 Management of Head Trauma and Traumatic Brain Injury 113
CPG 9.4 Management of Chest Trauma 115
CPG 9.5 Management of Abdominal Eviscerations 117
CPG 9.6 Management of Pelvic and Long Bone Fractures 118
CPG 9.7 Management of Suspected Spinal Injuries 121
CPG 9.8 Management of Burns 124
CPG 10.1 Management of Heat Related Injury and Heat Stroke 126
CPG 10.2 Management of Cold Related Injury 128
CPG 10.3 Management of Envenomation 130
CPG 10.4 Management of Submersion Injury 132
CPG 11 Management of Combative Patient 135
OBSTETRIC GUIDELINES
CPG 12 Clinical Approach to the Obstetric Patient 139
CPG 12.1 Management of antepartum complications 145
CPG 12.1.1 Management of Ectopic Pregnancy 146
CPG 12.1.2 Management of Threatened Miscarriage 148
CPG 12.1.3 Management of Placenta Abruptio & Previa 150
CPG 12.1.4 Management of Pre-term Labour 153
CPG 12.2 Management of Pre-eclampsia and Eclampsia 156
CPG 12.3 Management of Delivery and Associated Complications 159
CPG 12.3.1 Management of Imminent Delivery of the Newborn 160
CPG 12.3.2 Management of Breech Presentation 163
CPG 12.3.3 Management of Umbilical Cord Prolapse 167
CPG 12.4 Management of Post Delivery (or 3rd stage) Complications 169
CPG 12.5 Management of Maternal Cardiac Arrest 172
CPG 12.6 Management of Obstetric Trauma 175
CONTENTS
PEDIATRIC GUIDELINES
CPG 13 Clinical Approach to the Paediatric Patient 177
CPG 13.1 Management of Newborn and Newborn Resuscitation 187
CPG 13.2 Management of Paediatric Cardiac Arrest 191
CPG 13.3.1 Management of Acute Foreign Body Airway Obstructions in Paediatrics 197
CPG 13.3.2 Management of Croup and Epiglottitis
201
CPG 13.4 Management of Anaphylaxis in Paediatrics 205
CPG 13.5 Management of Paediatric Bronchoconstriction 208
CPG 13.6 Management of Paediatric Seizures 211
CPG 13.7.1 Management of Paediatric Symptomatic Bradyarrhythmias 215
CPG 13.7.2 Management of Paediatric Symptomatic Tachyarrhythmias 218
CPG 13.8 Management of Paediatric and Newborn Hypoglycaemia 221
CPG 13.9 Management of Paediatric Trauma 223
CPG 13.10 Management of Shock in Paediatrics 226
CPG 13.11 Paediatric Pain Management 230
CPG 13.12 Paediatric Procedural Sedation 233
CPG 13.13 Rapid Sequence Induction for Paediatrics 236
INTER-FACILITY TRANSFER GUIDELINES

CPG 14.1 Continuation of Previously Prescribed Medication 239
CPG 14.2 Use of Specialist Medication During Transfer 242
FORMULARY 243
Rapid Sequence Induction Quick Reference Guide 343
Extended Pharmacopeia Retrieval Services 344
Medication Privileges 346
Acknowledgments 347
CPG FLOWCHART
CPG 2.1 ADULT FOREIGN BODY AIRWAY OBSTRUCTION 14

CPG 2.2 MANAGEMENT OF UPPER AIRWAY SWELLING IN ADULTS 18
CPG 2.2.1 MANAGEMENT OF ANAPHYLAXIS IN ADULTS 21
CPG 2.3 RAPID SEQUENCE INTUBATION DRILL 24
CPG 3.1 ADULT ACUTE BRONCHCONSTRICTION MANAGEMENT 37
CPG 3.4 MECHANICAL VENTILATION 44
CPG 4.2 ACUTE CORONARY SYNDROMES 56
CPG 4.2 ACS 12-LEAD ECG DECISION TREE 59
CPG 4.3 MANAGEMENT OF ACUTE PULMONARY OEDEMA 60
CPG 4.4 MANAGEMENT OF ADULT SEPSIS 63
CPG 4.5.1 MANAGEMENT OF ADULT SYMPTOMATIC BRADYARRHYTHMIAS 65
CPG 4.5.2 MANAGEMENT OF ADULT SYMPTOMATIC TACHYARRHYTHMIAS 68
CPG 5.1 MANAGEMENT CEREBROVASCULAR ACCIDENT / STROKE 76
CPG 5.2 MANAGEMENT OF ADULT SEIZURES 80
CPG 6.3 SAFE SEDATION AND MONITORING IN ADULTS 88
CPG 9.7 MANAGEMENT OF SUSPECTED SPINAL INJURIES 120
CPG 11 MANAGEMENT OF THE COMBATIVE PATIENT 134
CPG 12.1.4 MANAGEMENT OF PRETERM LABOUR 152
CPG 12.2 MANAGEMENT OF PRE-ECLAMPSIA AND ECLAMPSIA 155
CPG 13.1 RESUSCITATION OF THE NEWBORN 186
CPG 13.3.2 MANAGEMENT OF PAEDIATRIC UPPER & LOWER AIRWAY OBSTRUCTION 200
CPG 13.4 MANAGEMENT OF ANAPHYLAXIS IN PAEDIATRICS 204
CPG 13.5 PAEDIATRIC ACUTE BRONCHCONSTRICTION MANAGEMENT 207
CPG 13.6 MANAGEMENT OF PAEDIATRICS SEIZURES 210
CPG 13.7.1 MANAGEMENT OF PAEDIATRICS SYMPTOMATIC BRADYARRYTHMIAS 214
CPG 13.7.2 MANAGEMENT OF PAEDIATRICS SYMPTOMATIC TACHYARRYTHMIAS 217
CPG 13.13 PAEDIATRIC RAPID SEQUENCE INTUBATION DRILL 235
FORMULARY
Click on the drug name to go to that page
Adenosine 246
Adrenaline/ Epinephrine 249
Amiodarone 255
Aspirin (acetylsalicylic acid) 259
Atropine 261
Budesonide 264
Calcium Chloride 266
Clopidogrel 268
Dexamethasone 270
Dextrose (oral & IV) 272
Diclofenac 275
Diphenhydramine 277
Fentanyl 280
Furosemide 283
Glucagon 285
Glycerol Trinitrate - GTN (sublingual and IV) 287

Hydrocortisone 290
Ibuprofen 293
Ipratropium Bromide 295
Ketamine 297
Ketorolac 301
Magnesium sulphate 304

Methoxyflurane (Penthrox) 308
Metoclopramide 310
Midazolam 312
Naloxone 316
Noradrenaline 319
Ondansetron 321
Paracetamol 324
Paracetamol
Phenylephrine 327
Prochlorperazine (Stemetil) 329
Rocuronium 331
Salbutamol 333
Succinylcholine (suxamethonium) 337
Tranexamic Acid (TXA) 339
Vecuronium 341
ABBREVIATIONS
AAA Abdominal Aortic Aneurysm EtCO2 End Tidal Carbon Dioxide
ACS Acute Coronary Syndrome ETT Endo Tracheal Tube(s)

AF Atrial Fibrillation FiO2 Fraction of Inspired Oxygen
AIDS Acquired Immune Deficiency Syndrome GCS Glasgow Coma Scale
ant. Anterior GI Gastrointestinal
A-P Anteroposterior gm Gram
APH Antepartum Haemorrhage Hb, Hgb Hemoglobin

ARDS Adult Respiratory Distress Syndrome HIV Human Immunodeficiency Virus
ARF Acute Renal Failure h/o History of
AVPU Alert, Verbal, Painful, Unresponsive HR Heart Rate

(Neurologic Test)
HTN Hypertension
Bilat.or B/L Bilateral
hx History
BIPAP BI-Level Positive Airway Pressure
ICP Intracranial Pressure
BP Blood Pressure
IDDM Insulin Dependent Diabetes Mellitus
bpm Beats Per Minute
I:E Ratio Inspiratory/ Expiratory Ratio
BSA Body Surface Area
IHD Ischaemic Heart Disease
BVM Bag Valve Mask Resuscitator (Ambu
IM Intramuscular
BW Birth Weight
IMV Intermittent Mandatory Ventilation
Ca Cancer
Inj Injection
CAD Coronary Artery Disease
IPPV Intermittent Positive Pressure Ventilation
CHF Congestive Heart Failure
IV Intravenous
c/o Complains of
JVP Jugular Venous Pressure
COPD Chronic Obstructive Pulmonary Disease
kg. Kilogram
CPAP Continuous Positive Airway Pressure
KVO Keep Vein Open
CPR Cardiopulmonary Resuscitation
LBBB Left Bundle Branch Block
CRF Chronic Renal Failure
LBW Low Birth Weight
CSF Cerebrospinal Fluid
l/min Liters per Minute
C-spine Cervical Spine
LMA Laryngeal Mask Airway
CT Scan Computerized Axial Tomography Scan
LMP Last Menstrual Period
CVA Cerebrovascular Accident
LOC Level of Consciousness
CVS Cardiovascular System
LVF Left Ventricular Failure
D5W 5% Dextrose in Water
MAP Mean Arterial Pressure
DDx Differential Diagnosis
MAS Meconium Aspiration Syndrome
DKA Diabetic Ketoacidosis
max Maximum
DNAR Do Not Attempt Resuscitation
MDI Metered-Dose Inhaler
DVT Deep Venous Thrombosis
mg Milligram
Dx Diagnosis
Ml Myocardial Infarction
ECG Electrocardiogram(s)
min Minute
ECHO Echocardiogram
ABBREVIATIONS
ml Milliliter PVC Premature Ventricular Contraction
mmol Millimoles RBBB Right Bundle Branch Block
mV Millivolt RBS Random Blood Sugar

N&V Nausea & Vomiting RHF Right Heart Failure
NA Not Applicable RR Respiratory Rate
NaCl Sodium Chloride RSI Rapid Sequence Induction

NAD No Abnormality Detected RTA Road Traffic Accident
NGT Nasogastric Tube sec second
NIDDM Non-insulin Dependent Diabetes Mellitus SIDS Sudden Infant Death Syndrome
NSR Normal Sinus Rhythm SIMV

Synchronized Intermittent Mandatory
NRBM Non-Rebreather Mask Ventilation
NSAID Non-steriod Anti-Inflammatory Drug SL Sublingual (Under the Tongue)

NSTEMI Non-ST Elevation Myocardial Infarction SOB Shortness of Breath
O2 Oxygen SpO2 Oxygen Saturation via Pulse Oximetry
O2 Sat Oxygen Saturation STEMI ST-Elevation Myocardial Infarction
O/E On Examination SVD Spontaneous Vaginal Delivery
PAC Premature Atrial Contraction SVT Supraventricular Tachycardia
PAF Paroxysmal Atrial Fibrillation T Temperature

PCI Percutaneous Coronary Intervention TV Tidal Volume
PE Pulmonary Embolism Tx Treatment
PEEP Positive End Expiratory Pressure URTI Upper Respiratory Tract Infection
Pupils Equal, Round, Reactive to Light UTI Urinary Tract Infection

PERRLA
and Accommodation VF Ventricular Fibrillation
pH Hydrogen Ion Concentration vol Volume
PID Pelvic Inflammatory Disease Vtach Ventricular Tachycardia

PIH Pregnancy Induced Hypertension wk Week
PIP Peak Inspiratory Pressure wt Weight
PND Paroxysmal Nocturnal Dyspnea x/7 number of days

po per oral, by mouth x/12 number of months
PPH Post Partum Hemorrhage x/52 number of weeks
prn As Often as Necessary yrs Years
PROM Premature Rupture of Membranes > Greater Than
pt Patient ≥ Greater Than or Equal To
PTB Pulmonary Tuberculosis < Less Than
PTL Pre-term Labour ≤ Less Than or Equal To
DO NOT USE ABBREVIATIONS
Abbreviations and symbols Potential problem Use instead
HS, hs, hs could mean “half strength” or “bed time” half strength or bed time
od could mean “right eye” or “once daily” right eye or once daily
dc could mean “discontinue” or “discharge” discontinue or discharge

u (unit) mistaken for “0” (zero), the number “4” (four) or “cc” write “unit”
iu (international unit) mistaken for iv (intravenous) or the number 10 (ten) write “international unit”
trailing zero ( x.0 mg )* lack of
decimal point is missed write x mg write 0.x mg
leading zero ( .x mg)
CPG 1
CLINICAL APPROACH TO AN ADULT

MEDICAL PATIENT
The adult patient is defined as a person of 14 years or older.

Their chief complaint should not be from physical injury.
The vital sign monitoring requirements in this guideline

should be applied as a minimum standard to all identified
patients by all Ambulance Paramedics (AP) and
Critical Care Paramedics (CCP).
Consent should be obtained prior to performing any

assessments, unless consent is implied.
TABLE 1. NORMAL VITAL SIGN RANGE FOR ADULT PATIENTS
VITAL SIGN NORMAL RANGE

Blood Pressure Less than 140 systolic and 90 diastolic
Pulse Between 50-100 beats per minute
Respiratory Rate 12-20 breaths per min, there may be a degree of hyperventilation
Temperature 36-37.6ºC
RBS 4-6.7 mmol/L
CPG 1 PAGE 1
BACK TO TABLE OF CONTENTS
INITIAL ASSESSMENT
RESPONDER SAFETY AND SCENE SIZE-UP

1. Standard and Environmental Precautions (see SOP 2.1)
2. Observe for any dangers (dangers to crew, patient, bystanders)
3. In patients with fever, cough or travel history to high-risk countries, consider risk of infectious dis-
eases.
PRIMARY SURVEY
1. Assess level of consciousness (AVPU) as per CPG 1.1:
If unresponsive:
 and no signs of breathing or has agonal breathing: refer to CPG 4.1 (adult medical cardiac
arrest)
 with signs of breathing (not agonal breathing) assess Airway as per CPG 1.2 (Airway and Re-
spiratory Status Assessment) and then Breathing as per CPG 1.2.
If Alert or responding to Voice or to Pain:
 Assess Airway as per CPG 1.2 and then assess Breathing as per CPG 1.2
2. Assess Circulation as per CPG 1.3 (Perfusion Status Assessment)
ABC life threats must be treated as soon as they are

found, before moving on to any further assessment.
AP staff should call for CCP assistance if
ABC life threat is present.
3. Confirm the Chief Complaint

(Chief complaint: The chief complaint is the main reason the person called for the ambulance. It
may not actually be the primary cause of the problem but merely a secondary symptom (like vomit-
ing in acute coronary syndrome without chest pain). It should give you a good starting point for the
problem-focused history).
4. Begin simultaneous process of asking a problem focused history and undertaking a focused as-
sessment:
Brief Problem Focused History: This is focused initially on the chief complaint and any suspi-
cions that flow from the chief complain
CPG 1 PAGE 2
 Use a structured system (eg. SAMPLE)
 Consider other causes (differential diagnoses) of chief complaint and focus your questions to
include or exclude various conditions.
 Use questions to rapidly identify any potentially life threatening problems so treatment can be
initiated rapidly.
Problem Focused Assessment: This assessment includes obtaining a basic set of vital signs
and performing a focused physical exam based on the patient’s chief complaint. A basic set of vital
signs should be obtained as soon as possible in all patients.
The basic set of vital signs is comprised of the following:
 Pulse rate
 Respiratory Rate
 Blood Pressure
 SpO2
 Temperature
 Level of Consciousness
In addition to obtaining a basic set of vital signs, the following assessments should be performed
during the primary survey when indicated:
 Measure an RBS in any patient where the glucose level may be a cause of their symptoms.
(Example: patients with an altered level of consciousness, weakness, dizziness, stroke-like
symptoms, history of diabetes, seizures, fasting, etc.)
 Undertake a pain assessment (if pain present use Visual Analogue or Numeric Scale – CPG
6.1)
 12-Lead ECG (CPG 4.2)
 FAST Exam (CPG 5.1)
Assess the relevant parts of these various systems based on patient chief complaint and brief
focused history:
 Head and neck: AVPU, pupil size and reaction time, unusual breath odours, distended neck
veins in the sitting patient.
 Chest: Abnormal movement symmetry, breath sounds on auscultation (normal, wheezing,
crackles or absent), use of accessory muscles of the upper chest, neck and abdomen. Pres-
ence of cough. (Initiate 12-Lead ECG if indicated)
 Abdomen: Rigidity, tenderness, distension.
 Limbs: Swelling, pulse quality, temperature to touch, grip or push strength.
CPG 1 PAGE 3
QATAR EARLY WARNING SCORE:
Once the basic set of vital signs is obtained, a QEWS score can be calculated. A score of 4 or more is
a marker of an increased risk to the patient, considering patient condition, request CTL consult:
HMCAS QEWS TABLE

QEWS 3 2 1 0 1 2 3
RESPIRATORY RATE <8 9–20 21–25 26–35 > 36
HEART RATE < 31 31– 40 41– 50 51–100 101–110 111–129 > 129
SYSTOLIC BP < 70 71– 89 90 –109 110–179 180–199 > 200
TEMPERATURE C(36ºC) N(36º–38ºC) H(> 38ºC)
SpO2 on Air < 90% 90 – 92% 93 – 94% ≥ 95%
AVPU U P V A
A score of 4 or more is a marker of an increased risk to the patient. TOTAL =
INITIAL MANAGEMENT
Initiate immediate life support therapy as required:

1. In patients responding to Pain or Unresponsive, open airway or turn lateral, clear (suction if need-
ed) and maintain airway using basic or advanced interventions as needed.
2. Provide oxygen as per CPG 3.3 if indicated.
3. Calm and reassure patient, place in position of comfort/ appropriate for patient condition.
The situation report to NCC should include the following:

1. Identify your unit.
2. Exact location (note any dangers encountered).
3. Patient age and gender (also include patient status i.e. VVIP etc.)
4. Provisional diagnosis or chief complaint (e.g. cardiac chest pain, severe respiratory distress etc.)
5. QEWS score (abnormal vital signs reported to CTL)
6. If CCP / Delta / other services (Police, Civil Defense) support is required.
HMCAS CLINICAL PRACTICE GUIDELINES Version 1.4 2019 CPG 1 PAGE 4

Based on patient severity and time critical nature
of their condition, consider early transport
and/ or rendezvous with CCP enroute,
undertake ongoing assessment and treatment enroute.
Time critical adult medical patients are as follows:

1. Actual: patients who require urgent hospital based intervention (eg. ACS and CVA)
2. Emergent: patients who require immediate on-scene intervention (by AP and/ or CCP)
3. Non-time critical
ONGOING ASSESSMENT AND MONITORING
1. Complete detailed history (full AMPLE history)

2. Complete relevant clinical examination (as required)
3. Ongoing communication with the patient and family
4. Regularly reassess vital signs based on the following:
 For transported patients a minimum of 2 sets of basic vital signs (RR, BP, HR, SpO2,
LOC) and pain score assessment unless the patient refuses. Note: performance of basic
life-saving interventions such as chest compressions, hemorrhage control, clearing the airway
or moving the patient into the hospital or out of an immediately dangerous environment etc.
should not be delayed or interrupted in order to obtain vital signs.
 Vital signs should be obtained at least every 15 minutes
 A basic set of vital signs should be obtained before and after medication administration. Note:
Life-saving medication should never be delayed in order to obtain a full set of vital signs.
(Example: if a blood pressure or SpO2 cannot be obtained due to poor perfusion in the case
of life-threatening anaphylaxis, IM Adrenaline administration should not be delayed. Proper
clinical judgement must be used in these cases.)
5. Continuous SpO2 and ECG monitoring, in addition to basic vital signs monitoring, is required until
handover at the receiving facility in the following cases:
 Patient complaining of chest pain, shortness of breath, or who has an altered level of con-
sciousness
 Patients who have received medications with sedative or paralytic effects (narcotics,
benzodiazepines, dissociative agents, paralytic agents) by any route also to have ETCO₂
continuously monitored.
 Patients who have received IV medication.
 Any patient in whom an invasive airway has been placed also to have ETCO₂ continuously monitored.

The above list is not all inclusive. Good clinical judgement must be used when deciding whether to
provide continous SpO2 and ECG monitoring. A cautious approach is recommended
6. Continuous 12-Lead ECG monitoring during transport is recommended in any patient complaining
of chest pain who receives a 12-Lead ECG, all 12 Lead cables must remain in place during
transport. This is regardless of whether the initial ECG is interpreted as normal. If the moni-
tor prints a new 12-Lead on its own (without you pushing the 12-Lead button), the CTL or the CCP
should be advised immediately.
 If a STEMI has been diagnosed, remove 12-lead precordial leads and place defib pads. If
unable to place defib pads due to patient request or modesty, make sure the defib pads are
prepared and near the patient.
7. Continuous EtCO2 monitoring is mandatory in the following circumstances:
 any time an invasive airway is placed or maintained (LTA, ETT, Cricothyrotomy),
 any time fentanyl or midazolam or ketamine are administered to a patient.
 when a paralytic agent is administered.
 when non-invasive ventilatory support is provided (CPAP, BVM), if time allows.
 For the CCP, awake EtCO2 monitoring utilizing a specialized nasal cannula should be
considered in any patient with moderate to severe respiratory distress.
8. For non-emergent scheduled transfers (those not generated by 999 calls) such as PTS
cases, vital signs need only be observed if the patient appears unwell, develops a new complaint
during transport (chest pain, shortness of breath, etc.) or if the family or patient requests.
Notification of a change in a patient’s condition should be made to NCC as appropriate. Request
assistance if required and provide stabilising care in line with scope of practice.
Remember, this is a guideline and the appropriate interval

for vital signs observation is dependent on the patient’s
condition and is weighed against the need to perform higher
priority interventions.

ONGOING MANAGEMENT
1. Consider establishing IV line for drug access or fluid therapy if required – choose an appropriate
size of cannula for purpose of IV line: smaller cannula for drug access (20g or 18g) and large bore
for fluid administration (16g or 14g).
2. Specific Management (as per specific Clinical Practice Guidelines)
TRANSPORT CONSIDERATIONS
1. Ensure scene time is appropriate for patient presentation.

2. Initiate transport after immediate life-saving interventions in time-critical patients. If the CCP is not
on scene meet the CCP en route as per SOP 4.8h
3. Transport to an appropriate facility with pre-notification by CTL if required (as per each CPG and
pathway)
4. Consider time to hospital versus time to rendezvous with CCP (do not unnecessarily delay trans-
port)
5. If the patient refuses transport or further care, follow SOP 4.8d for on-scene discharge.
6. Record final assessment at hospital and ensure patient is handed over to the appropriate staff –
using SOP 4.8b
The clinical approach is to be applied to all patients

as a minimum level of care. The only exception is the patient
with an immediate life-threatening condition,
as identified by the primary survey, which requires
immediate intervention (eg. CPR)
Consideration should be given in the clinical approach

to geriatric patients. All drug and fluid therapy described
in the specific guidelines below need to carefully considered
in the presence of co-morbidities: renal, cardiac,
chronic respiratory and neurological deterioration.

CPG 1.1
CONSCIOUS STATUS ASSESSMENT
The conscious state of a patient needs to be assessed based on their response to stimuli – either
voice or if required pain, in a way that is rapid, reproducible and objective. This enables trends to be
followed as different medical professionals are using the same basis for their assessment.
Primary assessment of a patient’s level of consciousness is undertaken using the AVPU scale. The
level is based on the patient’s BEST response that is maintained:
A: Alert person is aware of who they are, where they are and time (day of the week,
approximate time of day – morning, afternoon, night).
V: Verbal person appears drowsy, confused or unresponsive but then responds when you
talk to them or to a louder shout.
P: Pain person appears unresponsive but responds with movement or groaning when a
painful stimulus is applied to them.
U: Unresponsive the person does not respond to any stimulus (verbal or painful).
COMMON CAUSES FOR UNCONSCIOUSNESS:

There are four primary causes of an altered state of consciousness in adults:
1. Inadequate supply of the brain’s metabolic needs, e.g. hypoxia, hypoglycemia, electrolyte imbal-
ances, hypotension, etc.
2. Chemically induced alteration of brain function, e.g. drugs, alcohol, toxins, etc.
3. Direct trauma to brain tissue (eg. traumatic brain injury, CVA, cerebral infections)
4. Alterations in brain function or structure (eg. seizures, dementia, Alzheimer’s)
HMCAS CLINICAL PRACTICE GUIDELINES Version 1.4 2019 CPG 1.1 PAGE 8
CPG 1.2
AIRWAY AND RESPIRATORY STATUS

ASSESSMENT
Airway assessment is undertaken to identify any potential or actual life-threatening conditions. The
assessment of the airway is based on level of consciousness and the ability of the patient to talk.
Assessment of the respiratory system helps to identify respiratory or oxygenation problems and helps
to grade them from normal to severe respiratory distress, so the correct level of treatment can be
initiated.
AIRWAY STATUS
In the conscious patient, if they can talk, their airway is patent, airway assessment should be consid-
ered only when the patient is unable to talk properly or at all or has a decreased LOC, or there are
abnormal sounds from the airway (e.g. in FBAO and airway swelling with stridor). In the patient who
is not Alert (AVPU), the airway should be assessed as it may become occluded by the position of the
tongue, by secretions, blood or vomitus.
RESPIRATORY STATUS
What defines normal respiratory status?
1. The general appearance is calm and alert.
2. The patient is able to speak in full sentences with clear and steady speech.
3. On auscultation the chest is clear with good air entry on both lung fields.
4. Respiratory rate of 9-20/min
5. Regular, even cycles of breathing with normal chest movements.
6. HR = 50-100 bpm
7. Skin = warm, pink and dry
8. SpO2 ≥ 95%
9. EtCO2 between 35 and 45mmHg
What defines mild respiratory distress in a patient?
1. Alert but may be mildly anxious, noticeable chest movement (increased respiratory effort).
2. The patient is able to speak full sentences.
3. They are able to cough on request.
4. In asthma: they will have a mild expiratory wheeze and a slightly prolonged expiratory phase of
breathing.
5. In heart failure: there may be some fine crackles at the bases of the lungs.
6. Respiratory rate of >20 and < 24 per minute.
7. HR = 50-100 bpm
What defines moderate respiratory distress in a patient?

1. Alert or irritable, may appear distressed or anxious, obvious chest movements and using accesso-
ry muscles.
2. Able to speak short phrases.
3. Able to cough on request.
4. In asthma: there may be both expiratory and inspiratory wheezing.
5. In heart failure: crackles from the bases to the midzone of the lungs bilaterally, sometimes with
wheezing.
6. Respiratory rate will be 24-29/min
7. HR = 100-120 bpm
What defines severe respiratory distress/ life-threat in a patient?

1. These patients are compromised in more than one system and if not treated immediately they may
deteriorate quickly to death.
2. May be drowsy, agitated or unresponsive with obvious respiratory distress, fighting to breathe.
They can eventually progress to exhaustion and respiratory arrest.
3. Often unable to speak at all, or can speak a few words only.
4. Unable to cough effectively.
5. In asthma: may have weak expiratory and inspiratory wheezing, or a silent chest as they are mov-
ing too little air to produce a wheeze – THIS IS A LATE SIGN.
6. In heart failure: will present with audible bilateral crackles.
7. In an upper airway obstruction, may have inspiratory stridor.
8. Will be using accessory muscles, have marked or weak chest movements, intercostal retraction
and possible tracheal tugging (trachea pulls inwards on breathing).
9. Respiratory rate will be > 29 or < 8/ minute
10. HR ≥ 120 bpm – BRADYCARDIA IS A LATE SIGN OF BEING NEAR TO DEATH.
11. Skin is pale, sweaty and may be cyanosed.
RESPIRATORY STATUS ASSESSMENT TABLE

Mild Moderate Severe/ Life-threatening
General Calm or mildly anxious Anxious or distressed Anxious, distressed, fighting to

appearance breathe, exhausted, unrespon-
sive
Speech Full sentences Short phrases only Single words or unable to speak
Breath sounds Asthma: expiratory Asthma: expiratory wheeze Asthma: expiratory +/- inspirato-
wheeze +/- inspiratory wheeze. ry wheeze. May be silent – LATE
SIGN
HF: fine, basal crackles HF: basal to midzone
crackles, may have HF: full field crackles
wheeze
Upper airway obstruction: Inspi-
ratory stridor
Respiratory rate > 20/ min 24-29/ min > 29 or < 8/ min (LATE SIGN)
Respiratory Slightly prolonged expira- Prolonged expiratory Prolonged expiratory phase

rhythm tory phase phase
Effort Slight increase in chest Marked chest movement Marked chest movement using
movements using accessory muscles accessory muscles and tracheal
tugging or poor respiratory effort
Heart rate 50-100 bpm 100-120 bpm >120 bpm, bradycardia is a

LATE SIGN
Level of con- Alert but anxious Irritable with some distress Agitated, drowsy or unconscious
sciousness with marked distress
CPG 1.3
PERFUSION STATUS ASSESSMENT

To assess perfusion status we need to consider the state of the cardiovascular system (heart rate,
blood pressure and volume status) and its effect on some easy to assess key end organ functions
(CNS – level of consciousness and skin condition: colour and temperature).
The perfusion assessment table represents a graded progression from adequate perfusion to no per-
fusion.
When assessing perfusion in an adult patient, other factors may affect your observations, and these
needs to be accounted for. For example:
1. The environment: extremes in ambient temperature may affect the skin.
2. Anxiety and activity: may affect heart rate, blood pressure and the many causes of altered con-
sciousness/ unconsciousness.
3. Conscious status: may be affected by factors other than perfusion such as; hypoxia, hypoglycae-
mia, head injuries and toxins/ overdoses (alcohol, drugs etc).
The perfusion status assessment should be taken in context with:
1. The patient’s presenting problem.
2. The medication the patient may have taken.
3. Their response to treatment.
4. The trends shown through repeated observations.
5. The patient’s medical history.
PERFUSION
What defines adequate perfusion in the adult?

All parameters are within acceptable limits:
1. Alert and orientated to person, place and time.
2. Resting heart rate between 50-100 bpm.
3. Blood pressures: Systolic BP: 90-140 mmHg, Diastolic BP: 60-90mmHg and MAP 60-105mmHg
4. Skin: warm, pink and dry
What defines inadequate perfusion?
Early signs of inadequate perfusion (early shock) include the following:
1. Early altered conscious state with irritability, drowsiness, confusion or agitation.
2. HR <50bpm OR >100bpm with weak or absent peripheral pulses.
3. Systolic BP 60-90mmHg
4. Skin: cool, pale or clammy
What defines extremely poor perfusion?

Late signs of inadequate perfusion (late shock) include the following:
1. Significantly altered consciousness state with patient likely to only respond to pain or is unrespon-
sive (AVPU)
2. HR <40bpm OR >120bpm with no peripheral pulses, central pulses may be weak.
3. Systolic BP < 60mmHg OR unrecordable
4. Skin: cold, pale, mottled (red and pale spots) or clammy
What defines no perfusion?

This is characterized by unconsciousness, lack of breathing and no pulses.
1. Unresponsive with no breathing or only agonal breathing (very slow and irregular with gasping,
snoring or grunting sounds).
2. Absence of palpable central and peripheral pulses.
3. BP unrecordable.
4. Skin: cold, pale and clammy
PERFUSION STATUS ASSESSMENT TABLE

Level of Conscious- Heart rate BP (systolic) Skin condition
ness and temperature
Adequate Alert and orientated 50-100 bpm > 90 mmHg Warm, pink, dry
Inadequate Irritable, agitated, drowsy < 50 OR > 100 bpm 60-90 mmHg Cool, pale clammy
or confused
Extremely Poor Responsive to pain or < 40 OR >120 bpm < 60 mmHg Cool, pale clammy
unresponsive
No Perfusion Unconscious Absence of palpable Unrecordable Cool, pale or cya-
pulses nosed and clammy
CPG 2.1 ADULT FOREIGN BODY AIRWAY OBSTRUCTION
Assessment Reminders Other conditions to consider
 ARE YOU CHOKING?  Airway Swelling

 Can you speak?  Stroke with aphasia
 Can you cough?
 Chest thrusts/ chest compressions

C
O  Check airway
M  Remove obstruction ONLY if seen
P  Unable to talk
L or cough
E  Unconscious
T  Visualisation with laryngoscope and
E removal with Magills forceps
 Cricothyrotomy
C  Encourage to cough
O
 Apply 5 back-slaps - check after each
M  Unable to talk
P or cough  No relief, 5 rapid abdominal thrusts
L  Continue alternating back-slaps and
E  Conscious
T
abdominal/ chest thrusts until obstruction
E relieved or unconscious
P
A  Able to talk
R (hoarse)  Encourage to cough
T
I  Able to cough  Monitor for complete obstruction
A  Conscious
L
If patient has complete airway obstruction, initiate transport and meet

CCP or supervisor en route, continue FBAO basic life support.
AP & CCP CCP
BACK TO TABLE OF CONTENTS CPG FLOWCHART
CPG 2.1
TIME CRITICAL INTERVENTION
ADULT FOREIGN BODY AIRWAY

OBSTRUCTION
MANAGEMENT AIM
To rapidly and effectively dislodge/ remove the FBAO and restore normal respiratory function and min-
imize the risk of further deterioration into apnoea and hypoxic cardiac arrest.
The clinical indicators which suggest the management aim is being achieved are the following:
1. Improved SpO2 levels (≥ 95%)
2. Vital signs returning to normal levels (RR, pulse, BP, SpO2, skin colour normalizing)
3. Patient able to cough forcefully.
ASSESSMENT CONSIDERATIONS
Recognition is vital to achieving the management aim. It is key to recognize this emergency rapidly
from acute myocardial infarction, syncope, seizure or any condition that may cause sudden respiratory
distress, cyanosis or loss of consciousness.
Some identifiable features of FBAO may include: coughing or gagging, pointing to or grasping the
neck or trachea area, sudden inability to speak, stridor, wheezing, cyanosis and syncope.
RECOMMENDED MANAGEMENT
1. Initial approach as per CPG 1: Clinical Approach to the Adult Medical Patient:
2. In the conscious patient, ask, “Are you choking?” The person’s reply will indicate the risk to the
patient: If they can audibly reply “yes” then airway is only partially obstructed, if they are unable to
speak, this will verify complete airway obstruction.
SIGN PARTIAL OBSTRUCTION COMPLETE OBSTRUCTION
“Are you choking?” “Yes” Unable to speak, may nod
Cannot breathe/ wheezy breathing/
Can speak, cough, breathe silent attempts to cough/ uncon-
sciousness
3. In a conscious patient with partial or complete airway obstruction:

 Encourage the patient to cough and monitor for deterioration to ineffective cough or until the
obstruction is relieved.
 If the obstruction is not relieved, apply up to five back slaps, checking after each back slap if
the obstruction has been relieved.
Cautionary Point:
The aim is to relieve the obstruction with each backslap
rather than necessarily having to give all five.
 If five back slaps do not relieve the airway obstruction, give up to five abdominal thrusts rapidly.
 Chest compressions should be used for patients who are obese or pregnant or when the rescu-
er is unable to encircle the victim’s abdomen.
 If the obstruction is still not relieved, continue alternating five back slaps with five abdominal
thrusts or chest thrusts until relieved, or assistance takes over.
4. If at any stage the patient becomes unconscious:

 Support the patient and lower carefully to the ground.
 Immediately begin chest compressions in the manner you would do CPR.
 DO NOT FEEL FOR A PULSE.
 Compressions are performed at a ratio of 30:2
 Following each set of 30 compressions perform a head tilt chin lift and visually inspect if the
foreign body has been dislodged.
 Avoid blind finger sweeps as this may cause harm. Manually remove solid material in the air-
way only if it can be seen.
 Ventilations should be provided using the head tilt chin lift technique to open and maintain the
airway.
5. If these measures fail and the airway remains obstructed apply the following advanced life support
recommended management:
 Attempt to visualize the vocal cords with a laryngoscope.
 Remove any visible foreign material with a Magill’s Forceps and/ or suction if necessary.
 If the airway still remains obstructed undertake a cricothyrotomy.
In cardiac arrest as a result of FBAO, compressions are

performed at a 30:2 compressions to ventilation ratio.
(Manual and/or mechanical)
In cardiac arrest as a result of FBAO, a head tilt chin lift
technique is used to open and maintain the airway
during ventilation.
NOTE: DO NOT INSERT A SUPRAGLOTTIC AIRWAY DEVICE
DURING FBAO (LTA, OP Airways)
HMCAS CLINICAL PRACTICE GUIDELINES Version 1.4 ̀2019 CPG 2.1 PAGE 17
CPG 2.2 MANAGEMENT OF UPPER AIRWAY SWELLING IN ADULTS
 Stridor is a sign of partial upper  Foreign Body Airway Obstruction

airway obstruction  Upper respiratory tract infections
 Swelling of tongue, throat or face?  Anaphylaxis
 Hoarse voice?
 Dry cough and accessory muscle
use?
 Anaphylaxis? (CPG 2.2.1), Burns? (CPG 9.8)

 Adrenaline/ Epinephrine Nebulisation 5mg/ 5ml (1:1000) following CCP/CTL consult
 Consider early RSI (probable difficult airway) — prepare smaller

ETT
 Plan for cricothyroidotomy
Early rapid transport to hospital, WHILE providing treatment
AP & CCP CCP
BACK TO TABLE OF CONTENTS CPG FLOWCHART BACK TO TABLE OF CONTENTS
CPG 2.2
MANAGEMENT OF UPPER AIRWAY

SWELLING IN ADULTS
MANAGEMENT AIM
To identify the site and cause of the partial or complete airway obstruction and apply an appropriate in-
tervention to relieve/ limit the airway obstruction and improve ventilation and oxygenation. The clinical
indicators which suggest the management AIM is being achieved are the following:
1. Improved SpO2 levels (≥95%)

2. Vital signs returning to normal parameters.
1. Undertake a rapid assessment of the airway and breathing (breath sounds, use of accessory mus-
cles, ability to talk, cough and stridor).
2. Note any swelling of the tongue, throat or face.
3. Inspiratory stridor is usually caused by partial obstruction at the laryngeal level or above.
4. Speaking in a hoarse voice indicates swelling of the larynx.
5. Use of accessory muscles may suggest severe respiratory distress.
6. Coughing may suggest an upper and/or lower airway obstruction or infection.
Anaphylaxis (see CPG 2.2.1 on page 21)
SEVERE AIRWAY BURNS

May include soot in the nasal and oral cavities, singed facial hairs, cough with carbonaceous sputum,
hoarse voice, swollen lips, swollen tongue, changes in level of consciousness.
1. Consider risk of inhalational injury in any patient removed from fire in a confined space.
2. Immediately conduct a rapid airway assessment by asking patient to open their mouth and look for
signs of inhalational burns.
IDIOPATHIC ANGIOEDEMA
Describes a disease or condition that is without known cause, although when the idiopathic oedema
affects the larynx, there may be sudden internal throat swelling and presents similarly to anaphylac-
tic-type laryngeal oedema.
EPIGLOTTITIS AND TUMOURS OF THE THROAT

Infections and neoplasms can cause swelling in the upper airway leading to partial or complete ob-
struction of the larynx.
1. Initial approach as per CPG 1: Clinical Approach to the Adult Medical Patient.
2. Limit the swelling using Adrenaline/Epinephrine nebulization.
3. In ANAPHYLAXIS initiate management of anaphylaxis according to CPG 2.2.1
4. In SEVERE AIRWAY BURNS initiate the management of burns according to CPG: 9.8
5. Management of upper airway swelling due to IDIOPATHIC ANGIOEDEMA or burns or anaphylaxis
is the same.
6. Consider the need for securing the airway with endotracheal intubation (RSI – CPG 2.3). It is
important for early recognition of the potential for a difficult airway in patients who develop hoarse-
ness, tongue oedema, stridor, or oropharyngeal swelling.
Prepare a smaller-sized endotracheal tube since intubation

may be hampered by the presence of pharyngeal and
laryngeal oedema.
7. There is a high risk of a failed intubation and therefore a cricothyrotomy kit must be readily avail-
able, with the anatomical landmarks already prepared prior to the endotracheal intubation attempt.
8. The LT airway device MAY NOT work in patients with upper airway obstruction due to the swelling.
CPG 2.2.1 MANAGEMENT OF ANAPHYLAXIS IN ADULTS
 Sudden onset?  Idiopathic angio-oedema

 Likely cause? CVS, Respiratory,  CVS based syncope
GIT symptoms?  Asthma
 Airway involvement?  Stroke/ seizures
 Skin signs alone NOT anaphylaxis  Anxiety attacks
 First line medications:

 Adrenaline/ Epinephrine 1:1000 0.5mg IM – repeat after 5 min-
utes if required
 IV fluids: 500 –1000ml NS
 Second line medications
 Salbutamol Neb 5mg
 Upper airway swelling? Adrenaline/ Epinephrine Neb 5mg in 5ml
(1:1000) following CCP/CTL consult
 Ipratropium Bromide Neb 0.5mg
 Diphenhydramine IV/ IO/ IM 50mg (dilute for IV/IO)

 Hydrocortisone IV/ IO 200mg
 Adrenaline/ Epinephrine IV/IO infusion in cardiovascular collapse
 Using infusion device: mix 2mg 1:1000 with 18ml NS in 20cc
syringe – start at 2ml/hr (3.3mcg/min).
 Emergency interim infusion:
 Mix 1mg 1:10000 (1 pre-filled syringe) into 500ml NS. This
makes a 2mcg/ml solution.
 When using the standard 20gtts/ml drip set (double check
your drip set):
 30 drops per minute or 1 drop every 2 seconds = 3mcg/
min.
 Titrate to maintain a peripheral pulse.
 If Adrenaline is not effective, initiate a Phenylephrine infusion.
 If airway involved consider need for RSI (predicted difficult airway)

 Rapid transport if cardiovascular collapse persist or airway involvement
with inability to talk
AP & CCP CCP
HMCAS CLINICAL PRACTICE GUIDELINES Version 1.4 2019 CPG 2.2.1 PAGE 21
CPG 2.2.1
MANAGEMENT OF ANAPHYLAXIS
IN ADULTS
MANAGEMENT AIM
To identify anaphylaxis early and initiate interventions to terminate further histamine release, relieve
signs and symptoms and prevent life threatening complications. The clinical indicators which suggest
the AIM is being achieved are the following:
1. Reversal of upper airway compromise.
2. Relief of bronchoconstriction to keep SpO2 levels ≥95%.
3. Haemodynamic status returning to normal levels.
4. Prevention of delayed onset cardiovascular collapse.
Anaphylaxis is very likely if any of these three criteria are met:

1. Sudden onset of allergic response with involvement of skin and/or mucosa accompanied by airway
swelling, bronchoconstriction with respiratory distress and decreasing blood pressure. The ‘classi-
cal’ presentation is not the most common one. Skin and mucosal changes are absent in up to 20%
of cases, so is bronchoconstriction. Cardiovascular collapse can be the sole symptom.
2. Two or more of the following symptoms occurring rapidly after exposure to the likely allergen:
involvement of skin and/or mucosa, signs of respiratory distress, decreasing blood pressure or
end-organ dysfunction, and persistent gastrointestinal symptoms.
3. Decreasing blood pressure within minutes to several hours following exposure to a known aller-
gen.
4. Skin and mucosal changes ALONE are not a sign of anaphylaxis.
HMCAS CLINICAL PRACTICE GUIDELINES Version 1.4 2019

CPG 2.2.1 PAGE 22
RECOMMENDED TREATMENT
2. In a patient that meets the anaphylaxis criteria, initiate immediate management as follows:
 Administering FIRST line medication in cases of suspected anaphylaxis: Adrenaline/Epineph-
rine (1:1000) intramuscularly (IM) in the anterolateral aspect of the middle third of the thigh
muscle.
» This is to stop further histamine release, not to provide cardiovascular support at this
stage.
» Normal blood pressure and/ or tachycardia are NOT a contraindication to adrenaline.
» Repeated every 5 minutes according to the response.
3. If upper airway swelling is present consider nebulizing with Adrenaline/ Epinephrine (1:1000)
4. When establishing IV or IO – using large bore IV cannulae (16g or 14g):
5. Administer a fluid challenge of 500-1000ml NS if signs of cardiovascular compromise (repeat if
required)
6. Administer SECOND line medications:
 In patients with bronchoconstriction nebulize with Salbutamol according to CPG 3.1
 Ipratropium Bromide nebulized solution according to CPG 3.1
 Diphenhydramine IV/ IO/ IM (dilute and administer SLOWLY if given IV/ IO)
 Hydrocortisone IV/ IO/ IM
7. Adrenaline/ Epinephrine in circulatory failure (not cardiac arrest):
 In patients with cardiovascular collapse start Adrenaline/ Epinephrine infusion until cardiovas-
cular function is restored.
 Intravenous bolus of Adrenaline/ Epinephrine (in the context of anaphylaxis) is discouraged.
If using the emergency interim infusion, pay close attention

to the drip rate, blood pressure and peripheral pulse.
Assign one person to continuously monitor the emergency
interim infusion rate until the regular infusion device
is prepared.
8. Phenylephrine infusion if adrenaline is not effective.

9. CCP may administer diphenhydramine and/or hydrocortisone and handover to AP crew to transport patient
without CCP escort for stable MILD allergic reaction ONLY.
CPG 2.3 RAPID SEQUENCE INTUBATION DRILL
Assessment Considerations Other Considerations
AGE ≥ 14 years old  Do I have adequate access to the patient?

 Is there failure of airway patency/ protection?  Do I have an assistant?
 Is there failure of oxygenation or ventilation?  Do I have a bougie?
 Do I expect the clinical course to deteriorate?  Am I able to position for optimal laryngoscopy?
 Is this a potentially difficult airway?  Do I have a mechanical ventilator readily available?
 Do I have a backup BVM readily available?
 Laryngoscope (large and small handles) with working

for at least 94% SpO2 if possible. Leave EtCO2 nasal cannula in
cannula AND facemask. AVOID ROUTINE USE OF BVM! Aim
Provide at least 3 minutes of pre-oxygenation with EtCO2 nasal
light source and blades

place for apnoeic oxygenation during laryngoscopy.
Prepare equipment,
 Tested suction unit with suction catheter
Prepare yourself mentally,
Prepare for difficult/ failed intubation  Lubricated bougie
 Endotracheal tubes (3 size options available)
 Supraglottic airway device and video laryngoscope in
readiness
Position patient 20-25º head-up for  Surgical airway kit in readiness
optimal pre-oxygenation and laryngoscopy  Medications (checked and confirmed with partner)
Align the airway axes and place a pad under occiput
 Plan for mechanical ventilation
 Ensure bilateral IV lines are in place
Paralyze and induce the patient  Run in 500-1000ml NS (reduce in cardiac failure)
 Fentanyl up to 3mcg/ kg PLUS Ketamine up to 2mg/ kg
first, then Rocuronium 100mg (standard dose)
[Rocuronium 150mg for patient ≥100kg]
 Administer Fentanyl up to 3mcg/ kg PLUS Ketamine up
Perform External Laryngeal to 2mg/kg first then Suxamethonium 200mg; OR
Manipulation and/ or BURP
 For unstable patients (severe hypotension) reduce to
techniques as required
Fentanyl 1mcg/ kg PLUS Ketamine 1mg/ kg. Rocuronium
OR Suxamethonium dose remains the same.
 Check for jaw flaccidity before attempting laryngoscopy.
Place the ETT in the trachea and

confirm correct position  Use a bougie or video laryngoscope for the primary
attempt.
 Visualize the ETT go through the vocal cords.
 Auscultate EPIGASTRIUM/ LEFT LUNG/ RIGHT LUNG
Post-intubation  Confirm capnography waveform – apply oesophageal
management detector device
 Secure ETT with commercial device and note the mark-

ing at the teeth level
 Ensure that the ETT cuff is adequately inflated
 Place the patient on a mechanical ventilator as soon as
practically possible. Continuously monitor EtCO2
Maintain sedation and paralysis
 Ketamine 0.25 - 0.5mg/ kg every 15 - 20 min. as neces-
sary and Fentanyl 0.5mcg/ kg as necessary
st
 Rocuronium 1mg/ kg every 30-45 min following 1 dose
 Rocuronium 1mg/ kg within 6 - 8 minutes if Sux used
AP & CCP CCP

 Always prepare as if the airway is going to be difficult!
CPG 2.3
MANAGEMENT OF THE AIRWAY: RAPID

SEQUENCE INDUCTION FOR ADULTS
MANAGEMENT AIM
Rapid Sequence Induction of Anaesthesia is used to establish a definitive airway, protect the airway
and/ or manage oxygenation and ventilation if unable to do so by other means, based on an ad-hoc
risk-benefit assessment for the individual patient.
The clinical indicators which suggest the aim is being achieved are the following:
1. An increase in oxygen saturation level.
2. A regular capnographic pattern with target EtCO2 35-45 mmHg.
3. General improvement in vital signs.
It is imperative to recognize that the knowledge and skill required to successfully induce and maintain
an anaesthetic is not simply restricted to the psychomotor aspects of drug administration and tracheal
intubation.
RSI is a well-defined but high-stake procedure and can involve complex decision-making in practice.
Every effort has to be made to reliably achieve adequate anaesthesia, airway and ventilation while
avoiding negative side effects such as hyper/ hypotension, hypo/ hypercapnoea and hypoxia.
The procedure needs to be performed in a controlled manner and with margin of safety. On-scene
time targets take second place once the decision to RSI has been made. The practice of ‘RSI en
route’ is discouraged, as it requires working unrestrained in a moving vehicle.
Preparation is the key and the urge to rush must be resisted. Clear direction by the CCP and an orga-
nized team approach is required.
Considerations must take the need to minimize delays into account but in the absence of active un-
controllable haemorrhage, reducing scene time by minutes is unlikely to have any clinical benefit, but
will increase the risk of harm from a poorly conducted procedure.
INDICATIONS:
1. Failure of airway patency.
2. Failure of airway protection.
3. Failure of ventilation or oxygenation.
4. Anticipated clinical course/ humanitarian reasons.
5. To facilitate safe transportation.
ABSOLUTE CONTRAINDICATIONS:
1. Known hypersensitivity to any medication used in RSI.
2. Patient in whom cricothyrotomy would be impossible.
3. Patient in whom intubation would be impossible (e.g. severe upper airway obstruction).
4. Paediatric patients under the age of 14 years old.
5. Patient in peri-arrest (sometimes referred to as ‘Crash Airway’)
 Use basic airway maneuvers and ensure oxygenation (lifesaving)
 Place LT and address peri-arrest causes (quickly and adequately)
 Give Suxamethonium 200mg IVI or Rocuronium 100mg IVI (150mg in patient ≥100kg) if above
unsuccessful. Reattempt appropriate airway management. NB: Onset will be delayed due to
slow circulation time.
RELATIVE CONTRAINDICATIONS OF RSI:

1. Spontaneous breathing with adequate ventilation and airway maintenance.
2. Situations were optimal laryngoscopy will not be possible (e.g. environmental and human factors)
3. Patient in whom intubation would be difficult (e.g. a forced to act situation (rapidly deteriorating
patient) in the presence of a difficult airway)
CONSIDERATIONS:
The following criteria need to be considered when deciding if RSI is indicated and in the best interest
of the patient:
1. Time to definitive care
 Treatment and transport time – consideration given to time to undertake RSI compared to im-
mediate transport (and the risk of deterioration) to definitive care.
 Other than RSI, does the patient require a life or limb saving procedure immediately on arrival
in the Emergency Department?
2. Available Support (Human Factors)
 Is there a trained assistant to support the CCP if difficulties are encountered?
 Do other high priority procedures need to be carried out first or simultaneously e.g. chest de-
compression, haemorrhage control
3. Environmental Factors
 Risks on scene
 Location (desert, industrial site, residential, road way etc.)
PROCESS FOR IDENTIFYING DIFFICULT AIRWAYS:
Pre-hospital airways are assumed to be difficult until proven

otherwise by successful laryngoscopy.
If you decide to RSI, identify the risks for potential difficult airway using the mnemonic LEON as a use-
ful guide. The objective of an airway assessment is to formally assess for likely difficult laryngoscopy
(no surprises).
Even in combination, all assessment tools have a high false positive (predicted to be difficult but are
not) and false negative (predicted easy but are not) rate. Some of the assessment methods below
may be impractical in emergency cases and are only mentioned for completeness.
LOOK EXTERNALLY:
1. If the airway looks difficult, it probably is.
2. The external look specified here is for external evidence of lower facial disruption that might make
both intubation and mask ventilation difficult.
3. Look out for small mandible, short neck, large tongue, large teeth and retracted jaw.
4. Look for distortion of the anatomical landmarks for cricothyrotomy.
EVALUATE 3-3-2:
1. First 3 (Adequacy of oral access) Ability to accommodate three fingers between the incisors
2. Second 3 (Capacity of the mandibular space to accommodate the tongue on laryngoscopy)
 The thyromental distance is represented by the ability to accommodate three fingers between
the tip of the mentum and hyoid bone.
 More than or less than three fingers are both associated with greater degrees of difficulty in
visualizing the larynx.
3. The Final 2 (Identifies the location of the larynx in relation to the base of the tongue)
 Ability to fit two fingers between the hyoid bone and the thyroid notch.
 If significantly more than two fingers are accommodated, the larynx is distant from the base of
the tongue, indicating that it may be difficult to visualize the glottis.
 Fewer than two fingers may mean that the larynx is tucked up under the base of the tongue
and may be difficult to expose (anterior larynx).
OBSTRUCTIONS:
1. Upper airway obstruction should always be considered as a marker for a difficult airway.
2. Look out for:
 Muffled voice (hot potato voice)
 Difficulty swallowing secretions (because of pain or obstruction)
 Stridor
NECK MOBILITY:
The ability to position the head and neck (alignment of axis) is one the crucial factors necessary to the
achievement of the optimal laryngoscopic view of the larynx.
CONSIDER THE FOLLOWING ONCE THE DECISION TO RSI HAS BEEN MADE.
Always prepare as if the airway is going to be difficult.
The CCP should ideally perform the RSI with 360º access if possible but environmental or operational
conditions may require the procedure to be carried out in the back of the Alpha Unit with the patient on
the stretcher.
There are pros and cons for either, access and space to work or carry out other procedures in parallel
have to be weighed up against protection from the environment and spectators.
1. Initial approach as per CPG 1: Clinical Approach to the Adult Medical Patient, or CPG 9: Clinical
Approach to the Adult Trauma Patient.
2. PREPARATION – Complete RSI checklist
Pre-oxygenation: Pre-oxygenation is designed to increase the reserves of oxygen within the
lungs by denitrogenation of the functional residual capacity (FRC). This prolongs the apnoiec pe-
riod before hypoxaemia ensues. Maintenance of a patent airway during the apnoeic period allows
oxygen to reach the alveoli by the process of bulk flow. This occurs as a result of differences in
the volume of oxygen consumption and CO2 production and their respective solubility in blood.
Oxygen administered by nasal prongs together with a facemask, with a patent airway, prolongs the
time to desaturation. Owing to the negative pressure gradient that bulk flow causes, it is important
to maintain the application of continuous positive airway pressure via a tight fitting mask, in order
to reduce atelectasis.
» Consider 20-25 degree head up position unless a spinal injury is suspected.
» Pre-oxygenate with EtCO2 nasal cannula at 6L to 15L/min together with an oxygen face-
mask. Leave the nasal EtCO2 oxygen cannula in place as a means of apnoiec oxygenation
during laryngoscopy.
» Consider in-line manual stabilization. Some manipulation to achieve an adequate view will
be required but is unlikely to cause additional harm.
» Avoid routine use of the BVM as a means of preoxygenation
 Assessment/ monitoring
» Difficult airway assessment
» SpO2
» EtCO2
» HR
» BP
» ECG
 Access
» 2 x IV/IO secured, patent and accessible.
 Equipment
» Two laryngoscopes (large and small handles) with working light source and appropriate
blade sizes.
» Intubating bougie
» Endotracheal tube (+<1> size)
» Supraglottic airway device (LTA)
» Cricothyroidotomy kit
» Tested suction unit with hard and soft suction catheters
» Oxygen (ensure a spare is available if outside ambulance)
» Video laryngoscope (optional - may be used as primary laryngoscope)
 Position
» Ensure that the position of the patient and clinician enables optimum laryngoscopy. The
optimal head position is head slightly forward and hyper-extended (like sniffing morning air
or taking a sip of a drink). A pillow or other device to lift the head off the stretcher will be
required. Correct head position is probably the most crucial factor to increase likelihood of
easy laryngoscopy.
FAILED INTUBATION DRILL
1. Check head position
Unable to visualise cords 30 second drill

2. BURP (external laryngeal
manipulation)
3. Longer Blade
Unable to visualise cords Second Attempt
4. Blind bougie
5. LT
Unable to visualise cords 6. Consider 3rd attempt if

Safeguard saturation improved >95%
7. Consider intubation
via i-LT
Failed LT placement OR unable

to oxygenate > 80% with
LT or BVM Rescue 8. Surgical airway
» Move the patient to a better location/ position if you are not able to ergonomically carry out
laryngoscopy with ease. Ideally, raise the patient stretcher to waist-height of the intubator
so that laryngoscopy and endotracheal intubation are optimized.
 Medication
» Prepare drugs and decide on dose.
» Run 500-1000ml NS rapidly to prevent hypotension (Note: Use with care in cardiac failure)
 Team briefing prior to RSI should include your failed intubation drill and decision points. Decide
now at what point you will institute the different components of your failed intubation drill.
EXPLANATORY NOTES
The failed intubation drill is a continuation of the RSI drill i.e progression down the algorithm above is
‘part of the plan’.
Airway catastrophes after RSI have been shown to be principally due to the failure of switching from
intubation attempts to alternative ways of establishing an airway and oxygenation (task fixation), rather
than lack of technical proficiency.
For this reason the failed intubation plan mandates alternative techniques after two attempts and a
natural progression to the next step IRRESPECTIVE OF OXYGEN SATURATION.
A surgical airway is indicated when an LT placement fails to establish an airway (i.e when it is clear
that ET and LT have failed, regardless of saturation) OR LT and BVM fail to maintain oxygenation
above 80%.
The latter situation should prompt the practitioner to assure herself or himself first that other causes
for low oxygen saturations have been excluded if ventilation ‘feels’ adequate.
RECOMMENDED MEDICATION ADMINISTRATION

Anaesthesia for RSI and ventilation requires the three components of hypnosis, analgesia and paral-
ysis. Depending on the patient’s condition and pathology individual parts of the diagram below may
have to be altered.
The objective is to prevent awareness and maintain ‘haemodynamic stability’. Hypotension in brain
injury and tachycardia and hypertension in cardiac patients are harmful. Short term rise in intracranial
pressure is probably of less significance but excessive rise of blood pressure can precipitate a CVA or
increase intracranial bleed.
A patient with low GCS and normal to high blood pressure due to traumatic brain injury will need less
hypnosis but increased analgesia and paralysis.
A patient with low blood pressure but conscious will need hypnosis and paralysis but analgesia can be
reduced.
Invariably the practitioner will have to make some trade-off decisions and although a ‘Recipe Ap-
proach’ provides some degree of safety, adjustments will have to be made on a case by case basis.
Hypnosis
Pre-hospital
Anaesthesia
Analgesia Paralysis
The drugs and doses below are a starting guide and

operator discretion is required. As a principle, the
correct dose is the dose achieving the desired effect.
This may be much less but can also be significantly more
than mentioned here. For instance a drug and alcohol
naïve 50kg Nepalese national may require significantly
less sedative than a 100kg European, even on a
kilogram by kilogram basis.
FIRST LINE: PRIMARY INDUCTION AND PARALYSIS

1. Administer INDUCTION agent followed by saline flush
 STABLE PATIENTS (Blood Pressure normal to high range)
» Fentanyl up to 3mcg/ kg
» Ketamine 2mg/ kg
 UNSTABLE patients (Compensating or decompensating haemodynamics)
» Fentanyl 1mcg/ kg
» Ketamine 1mg/ kg
2. Administer PARALYTIC agent immediately AFTER induction agent followed by 5 ml saline flush.
 Rocuronium is the preferred paralytic agent.
 If Rocuronium is unavailable, use Suxamethonium for primary paralysis.
One of the most common reasons for difficult intubation

conditions is the failure to wait sufficiently long for
the muscle relaxant to take full effect. It is therefore
recommended to time 45 seconds after administration
of the muscle relaxant before checking jaw faccidity and
attempting laryngoscopy.
DELAYED SEQUENCE INDUCTION

The primary objective is to ‘get control’ in order to provide safe environmental and physiological condi-
tion prior to carrying out a traditional Rapid Sequence Induction.
Patients who are semi-conscious and agitated with or without a partially occluded airway and or hy-
poxia from gas exchange failure provide a particular challenge.
These situations are usually improved by the administration of a small amount of sedative and under-
taking basic airway management and oxygenation.
This will not only provide sufficient time to set up for RSI but also improve patient compliance with the
procedure and oxygenation, all culminating to provide safe conditions.
1. Give Ketamine IVI as soon as IV access established (if required even before taping IV down)
2. Provide two handed basic airway support and assisted ventilation with BVM as required.
3. Give further Ketamine or Midazolam or Fentanyl if required.
4. Set up for RSI.
5. Reduce dose of chosen induction agent as required.
MAINTENANCE OF ANAESTHESIA AND PARALYSIS POST INTUBATION
As mentioned above, drug doses are given as a guide. The dose and frequency of top ups depends
on the individual case and longer acting drugs are preferred. Frequent small doses are preferred over
less frequent large doses as they are less likely to lead to hypotension.
Patients who have been unconscious or hypotensive initially and consequently received a reduced
dose of a sedative for RSI are likely to improve with ventilation and resuscitation. This may require in-
creasingly more frequent or larger doses of a sedative to be administered en route in order to maintain
adequate anaesthesia.
1. Maintenance of sedation in aliquots as necessary (monitor for increase in heart rate, blood pres-
sure, lacrimation, swallowing, coughing/ gagging or interbreathing)
 Administer Ketamine every 15-20 minutes as necessary.
 Administer Fentanyl as necessary.
2. Maintenance of paralysis:
 Administer continous neuromuscular blockade (Rocuronium) within 30 minutes of primary
paralysis.
PLACEMENT WITH PROOF

1. Confirm three waveform cycles on capnography.
2. Auscultate the lungs to exclude endobronchial intubation.
3. Failed intubation: If in doubt, take it out! Insert LT, oxygenate, ventilate, regroup.
MONITOR FOR AND MANAGE POSSIBLE COMPLICATIONS POST RSI

Complications post RSI are usually related to a combination of drug induced hypotension (loss of
vasomotor tone), relative or absolute hypovolaemia and positive pressure ventilation, all conspiring to
reduce venous return resulting in hypotension and subsequently reduced blood flow through the lungs
causing desaturation.
Complication Action
1. Hypotension 1. Reduce tidal volume

2. Fluid bolus
3. Reduce respiratory rate in air trapping
4. Consider anaphylaxis
5. Vasopressors (Phenylephrine)
2. Desaturation 1. Check tube placement

2. Exclude pneumothorax
3. Check oxygen
4. Check blood pressure
5. Consider hypotension as cause
6. Consider anaphylaxis
3. High Airway pressure 1. Check ET tip position

2. Check ventilator tubing
3. Exclude pneumothorax
4. Suction ET tube
5. Reduce respiratory rate in air trapping
6. Consider part of pathology in lung
failure
7. Consider sign of anaphylaxis
In catastrophic deterioration carry out a Quick Check using the DOPE mnemonic:
Displacement
Obstructed ET or ventilator tubing
Pneumothorax
Equipment failure
Patients with a pre-existing pneumothorax WILL
eventually tension once CMV has been instituted. Tension
pneumothorax in the ventilated patient will present as
cardiovascular collapse. Pre-emptive decompression of a
pneumothorax is mandatory in ventilated patients.
POST INTUBATION MANAGEMENT

1. Secure ETT with commercial device and note the ETT depth using the marking at the level of the
teeth. (Tube depth is (12 + age in years/ 2), up to 20-22cm in adult women and 22-24cm in adult
men)
2. Ensure that the ETT cuff is adequately inflated. Deflate cuff until leak is detected, then reinflate
carefully until leak disappears.
3. Place patient on mechanical ventilator and commence ventilation according to CPG 3.4
4. Ensure continuous waveform capnography.
5. Consider gastric tube insertion, as it may improve ventilation if stomach distended from BVM venti-
lation (contraindicated in head injury).
6. BVM within reach as backup.
7. Monitor vital signs and manage hypotension aggressively.
8. Monitor ventilation variables (Pmax, and TV)
CPG 3.1 ADULT ACUTE BRONCHOCONSTRICTION MANAGEMENT
 Is patient using bronchodilators  COPD

 Recent lung infection?  Early onset pulmonary Oedema
 Is there wheezing on auscultation  Pneumonia/ URTI
 Respiratory Rate?  Pulmonary embolism
 Ability to talk?  Anaphylaxis
 Becoming drowsy or confused?
 Adrenaline/ Epinephrine 0.5mg 1:1000 IM for

anaphylaxis ONLY
 Salbutamol 5mg nebulised, use inline neb if
L decreased LOC
I
F
 Chest severe wheezing  250 ml Normal Saline IV infusion
E or silent  Ipratropium Bromide 0.5mg nebulized
 Talks in words or unable
T to talk
H  Hydrocortisone 200mg IV
 RR > 29
R  Magnesium 1-2g IV over 10 min. (if not re-
E  Decreasing LOC sponding to other therapy)
A
T  IV Salbutamol infusion: 250mcg over 10 min.
 Adrenaline/ Epinephrine 0.5mg 1:1000 IM for
anaphylaxis or asthma (give early if indicated)
 Salbutamol 5mg nebulised

S  Wheezing all lung fields  250 ml NS IV infusion
E
V  Talks in phrases  Ipratropium Bromide 0.5mg nebulized
E  RR 24-29
R
 Alert or drowsy
E  Hydrocortisone 200mg IV
M
O  Expiratory wheeze
D
E  Talks in full sentences  Salbutamol 5mg nebulized
R  RR < 24  Ipratropium Bromide 0.5mg nebulized
A
 Alert  250 ml NS IV infusion
T
E
 If patient has life-threatening symptoms, contact CTL/responding CCP

prior to initiating priority 1 transport.
AP & CCP CCP
CPG 3.1
MANAGEMENT OF ADULT ACUTE

BRONCHOCONSTRICTION (INCLUDING
ASTHMA, COPD AND ALLERGIC
REACTIONS)
MANAGEMENT AIM
To relieve the bronchoconstriction, decrease the work of breathing and improve ventilation and oxy-
genation. The clinical indicators which suggest the AIM is being achieved are the following:
1. Improved SpO2 levels (≥ 95% or ≥ 90% in COPD)
2. Vital signs returning to normal levels
3. Wheezing disappears and return of normal air sounds on auscultation
4. Improved patient breathing comfort (decrease feeling of shortness of breath)
1. Assess the history: previous breathlessness, cough, exposure to environmental pollutants (espe-
cially smoking), recent lung infections and family history of COPD.
2. Initial assessment: undertake a rapid assessment of the chest (breath sounds, use of accessory
muscles and symmetry of movement)
2. Treatment choice based on severity
 Moderate: Talks in full sentences, Respiratory rate < 24, Alert and orientated
» Nebulise the patient with Salbutamol (repeat if required) and Ipratropium Bromide
 Acute Severe: Moderate wheeze all lung fields, Talks short phrases, RR 24-29, Alert or drowsy
» Nebulise the patient with Salbutamol (repeat if required)
» Establish IV and consider administering 250ml IV Saline slowly
» Call for CCP assistance
» Nebulise with Ipratropium Bromide
» Add IV Hydrocortisone to patients with acute asthma and COPD exacerbation.
 Life Threatening: Chest silent or almost silent on auscultation, talks in words or no talking,
RR > 29, Decreased LOC
» Nebulise the patient with Salbutamol – repeat if required
» Establish IV and administer 250ml IV Saline slowly
» URGENT: Call for CCP assistance
» For life-threatening Asthma, consider Adrenaline/ Epinephrine 0.5mg 1:1000 IM
» Nebulise Ipratropium Bromide
» Add IV Hydrocortisone for patients with acute asthma and COPD exacerbation
» Add IV Magnesium to patients with acute severe bronchoconstriction unresponsive to
therapy.
» Add IV Salbutamol infusion in patient where air movement is too poor for nebulised therapy
to work quickly. IV Salbutamol is a secondary treatment after Magnesium.
3. CCP may administer hydrocortisone and handover to AP crew to transport patient without CCP escort
for stable MILD asthma ONLY.
CPG 3.2
MANAGEMENT OF SEVERE
RESPIRATORY INFECTION IN
ADULT PATIENTS
MANAGEMENT AIM
To improve oxygenation and ventilation thus preventing respiratory failure and to improve the cardio-
vascular status.
The clinical indicators which suggest the management aim is being achieved are the following:
2. Restoration of cardiovascular status in patients with associated dehydration.
3. Recognising impending respiratory failure and utilise selective ventilation to improve the respirato-
ry function.
1. Assess the history especially of breathlessness, cough, fever, and upper respiratory tract infec-
tions.
2. Initial assessment: undertake a rapid assessment of the chest (breath sounds, use of accessory
muscles and symmetry of movement, percussion)
3. Consider Acute Pneumonia if the following signs and symptoms are present: Tachycardia, Tachy-
pnoea, Fever, Breathlessness, Productive cough, pleuritic chest pain
4. In patients with cough and fever, consider risk of infectious disease such as MERS etc. take ap-
propriate precautions, eg. N95 face mask for crew, dust mask on patient, gloves, eye protection.
(refer to SOP 2.1)
2. If bronchoconstriction present, refer to CPG 3.1
3. Consider establishing an IV line and administering fluid boluses (250-500ml) to improve cardiovas-
cular status.
4. Consider analgesia using non-opioid analgesic Paracetamol (CPG 6.1) if chest pain is present.
5. If significant respiratory failure is present (tachypnoea > 30bpm and/or altered level of
consciousness and/or poor respiratory effort)
• Administer high flow oxygen regardless of SpO₂
• Call for CCP assistance
• Consider CPAP
• If airway protection required consider RSI (CPG 2.3) and mechanical ventilation
(CPG 3.4).
Remember to decontaminate all equipment including the

stretcher after every patient contact in line with SOP 2.3.
CPG 3.3
OXYGEN THERAPY
MANAGEMENT AIM
To treat and prevent hypoxemia and tissue hypoxia. Oxygen therapy should be titrated to achieve
target saturation levels.
The clinical indicators which suggest the management AIM is being achieved are the following:
1. SpO2 target range of 95% and above for acutely ill patients (except moderate to severe COPD
where SpO2 should be maintained around 90%)
2. An improvement in vital signs (see below) indicating an improvement in oxygenation and thus
decreasing sympathetic stress response to hypoxaemia.
1. Oxygen is a drug and thus should be administered only when it is indicated. Administration of oxy-
gen ‘just in case’ is discouraged.
2. Dyspnoea is not relieved by oxygen. Dyspnoea (air hunger) is a subjective symptom as a result of
many disease processes.
Many dyspnoeic patients are not hypoxic and many hypoxic

patients are not dyspnoeic.
3. Although oxygen is a safe drug it does carry some risks:
 V/Q mismatch: Parts of the lung may not be ventilated while still having perfusion (the mecha-
nism in COPD), which worsens the patients hypercarbia and may produce type II (hypercapnic)
respiratory failure (thus the recommendation for a lower SpO2 of around 90%).
 Absorption atelectasis: absorption of oxygen from alveoli with a high O2 content causes the
alveoli to collapse producing more V/Q mismatch.
 100% O2 has a higher density than air and thus increases the work of breathing – this may
decrease ventilation in exhausted patients.
 Oxygen administration in non-hypoxaemic acute myocardial infarction and strokes has pro-
duced increased mortality and infarct size.
4. The decision as to which method is used to administer oxygen is dependent on the individual pa-
tient’s clinical presentation and the response to the therapy – use the lowest oxygen concentration
to achieve the target saturation:
 Bag-Valve-Mask ventilation should be utilised in all non-breathing and hypoventilating patients.
Hypoventilation is defined as a patient whose ventilation is insufficient to maintain adequate
CO2 clearance (as measured by EtCO2). The oxygen flow rate should be set between 10 and
15 L/min to maintain the reservoir at 2/3 full.
 Continuous Positive Airway Pressure (CPAP) is used to increase oxygenation in patients who
have a reduced gas exchange from collapsed lung bases or impaired diffusion. It is mainly
used in patients suffering from low oxygen saturations despite high-flow oxygen in pulmonary
oedema, respiratory failure (Type I) or morbid obesity. It has limited value in COPD. CPAP is
to be used by CCPs only.
 Bi-level Positive Airway Pressure is CPAP with additional inspiratory support and is the pre-
ferred method for COPD patients who have reduced respiratory drive. COPD patients with
reduced level of consciousness require intubation and ventilation.
 High concentration reservoir mask is used to administer O2 percentages of around 70%. This is
a fixed percentage independent of the patient’s respiratory pattern. A flow rate of 10-15 L/min is
selected to prevent the non-rebreathing bag from deflation at high respiratory rates. A tight fit is
required for the device to work adequately. This is the device of choice initially for patients with
significant hypoxemia (SpO2 levels below 90%).
 Nasal cannula is utilised in patients with moderate hypoxemia (SpO2: 90-94%)and who are able
to breathe through their nose. Flow rates of between 2- 4 liters are used. Higher flow rates can
be used but this is very uncomfortable.
 Nebulisation mask is used to administer aerosolized medications and saline to patients requir-
ing bronchodilators or humidification of thick secretions. Flow rate for nebulization should be
at least 6L/min.
CPG 3.4 MECHANICAL VENTILATION
Non-Invasive Ventilation (CPAP)
 Connect the appropriate disposable ventilation hose.

 Connect oxygen source and ensure it is open. If using a portable bottle, ensure it
is full and arrange for replacement bottles early.
 Select correct size tight fitting mask
 Select CPAP and settings as follows:
» Change to NIV 'ON' (Settings screen 2/3 on Oxylog3000 Plus)
» Start with PEEP of 5mbar
» Start ventilation and hold mask on patient in a calm and reassuring manner
- do not rush the placement of the mask as this will increase agitation and
decrease success.
» If patient is comfortable, increase PEEP to 10mbar, if this reduces comfort,
reduce PEEP back to 5mbar. Keep PEEP setting with highest comfort.
» If the patient requires further support, increase ∆Psupp by steps of +5mbar up
to a maximum combined PEEP + ∆Psupp of 20mbar.
 Secure mask in place when tolerated by the patient -- continue to calm and reas-
sure as needed to facilitate success.
Invasive Ventilation (CMV or SIMV)
 Connect appropriate disposable ventilation hose

 Connect oxygen source and ensure open
 Turn ventilator on and run through check cycle with test lung
 Setting as per ventilation table
 Change setting based on patient clinical response
 All patient given paralytics should be placed on a mechanical

ventilator
AP & CCP CCP
CPG 3.4
MECHANICAL VENTILATION
MANAGEMENT AIM
To manage impending or progressive respiratory failure while limiting the risk of ventilator associated
lung injuries. Mechanical ventilation should be titrated to achieve target saturation and EtCO2 levels
utilizing tidal volumes of 6-8ml/kg and a respiratory rate matched to achieve normocapnoea. The clini-
cal indicators which suggest the AIM is being achieved are the following:
1. SpO2 target range of 95% and above for acutely ill patients.
2. EtCO2 levels used to guide ventilation to maintain normal or near-normal values (35-50mmHg).
3. Selection of an appropriate ventilatory mode and PEEP setting to limit peak airway pressures
while achieving appropriate saturation and EtCO2 values.
4. Preventing patient discomfort during the ventilation process utilizing appropriate sedation and if
required paralysis.
5. Once reversible causes such as pneumothorax, tube displacement or equipment failure have
been excluded values of up to 80 mmHg for EtCO2 and SpO2 as low as 88% can be accepted in
preference to increasing tidal volumes and exceeding recommended airway pressures in order to
achieve normal saturations or normocapnoea.
INDICATIONS FOR MECHANICAL VENTILATION
Indications for mechanical ventilation are the following:

1. Apnoea (cardiac and respiratory arrest)
2. Rapid Sequence Intubation
3. NIV (non-invasive ventilation), CPAP and BiPAP, are used when PEEP and pressure support may
potentially prevent atelectasis and resolve the hypercapnoea or respiratory muscle fatigue (COPD
and acute pulmonary oedema).
4. Hypoxaemic respiratory failure unresponsive to other modes of oxygen administration e.g.
Respiratory failure (type I or type II)
5. Failure of the respiratory muscles due to severe respiratory fatigue, sedative drugs or neuromus-
cular disorders as noted by tachypnoea, use of accessory muscles and poor ventilator effort. The
decision as to which method is used to administer oxygen is dependent on the individual patients
clinical presentation and the response to the therapy – use the lowest oxygen concentration to
achieve the target saturation:
6. Interfacility transfer of mechanically ventilated patients
VENTILATION MODES AND MANAGEMENT
Mechanical Ventilation requires using appropriate modes and settings to maximize oxygenation and
ventilation while limiting potentially harmful effects. The ventilation parameters and modes described
are for the Oxylog 3000 plus.
The modes of ventilation are as follows:
1. Intermittent Positive Pressure Ventilation (IPPV) or CMV (Control Mandatory Ventilation) – used to
ventilate non-breathing patients during respiratory arrest or paralysis. When turning on the trigger
function (setting trigger value) the mode changes to IPPV-Assist – this synchronises the ventilation
to any spontaneous breaths by the patient.
2. Synchronised Intermittent Mandatory Ventilation (SIMV) is used in spontaneously breathing
patients to support their breathing and volume synchronised with the patients own breathing as a
minimum. This avoids the patient ‘fighting the ventilator’ and ensures minimum ventilation in case
of apnoea, this mode can be used for the interfacility transfer of patients.
3. Pressure support ventilation (PSV) is patient triggered and flow cycled providing additional inspira-
tory pressure during other pre-set ventilation modes (CPAP or SIMV) in spontaneously breathing
patients, this mode can be used for the interfacility transfer of patients.
4. NIV (non-invasive ventilation) – CPAP (continuous positive airway pressure) and BIPAP (Bi-level
positive airway pressure) is used in non-intubated patients to provide additional respiratory support
with end expiratory pressure to prevent atelectasis.
SETTINGS USED FOR VENTILATION:

1. Respiratory rate and tidal volume. Together these control minute volume. A target window of 6 – 8
ml/kg IBW should be aimed for. Respiratory rate should be set to achieve near normocapnia,
however, higher than normal ETCO₂ levels are acceptable in polytrauma, asthma and post
cardiac arrest patient.
Height (cm) 150 160 170 180 190
Tidal volume 300 - 400 360 - 480 420 - 560 480 - 640 540 - 720
6-8 ml/kg
For expediency we use the same ideal body weight for men and women. A TV target window is given
for practical reasons.
1. PEEP: positive end expiratory pressure – increases partial pressure of gases in the alveoli in-
creasing oxygen exchange (i.e. improves saturation) and prevents alveoli and airway collapse.
PEEP will decrease venous return, which may be beneficial in some patients (APO) or detrimental
in other (Shock), the higher the PEEP the greater effect it has on venous return. A usual starting
setting is a PEEP of 5, which can be increased up to 10, which is rarely necessary.
2. Maximum inspiratory pressure (Pmax) – this setting is a safety feature that limits the maximum
airway pressure thus limiting risk of barotrauma. During the ventilation cycle, if the maximum pres-
sure is reached before the full tidal volume is given the remaining tidal volume is dumped and this
may lead to hypoventilation. In severe lung failure (pneumonia) Pmax may have to be increased to
achieve minimum tidal volumes. A normal setting is 30 but may have to be increased to 40 in ‘stiff
lungs’ such as severe pneumonia
3. Oxygen percentage from 40% to 100%
4. Inspiratory / Expiratory ratio – this sets the time ratio of inspiration to expiration. A normal setting
is a ratio of 1:2. The I:E Ratio is only given as information and set automatically by choosing a
respiratory rate
5. Trigger value for adults must be set at 3L/minute when required (SIMV, CPAP, IPPV-Assist).
6. Pressure Support setting in CPAP and SIMV (up to 10mbar). A normal starting setting for CPAP is
2.5 and increased in increments as tolerated and required.
RECOMMENDED VENTILATOR SETTINGS FOR COMMON CONDITIONS:
Setting Normal lungs Asthma/ COPD Pulmonary

oedema / ARDS
Resp Rate 8 - 12 bpm 5 - 10 bpm 12-15 bpm
Tidal Vol 6 - 8 ml/kg 4 - 6 ml/kg 6 - 8 ml/kg
Pmax 35 mbar 40 mbar 40 mbar
Ti:Te 1:2 1:4 Up to 1:1
PEEP 5 mbar 0 - 5 mbar Up to 10 mbar
Mode of Ventilation IPPV IPPV IPPV/ NIV
Oxygen % As required As required As required
MECHANICAL VENTILATION IN ACUTE SEVERE ASTHMA/COPD
Patients with acute severe asthma may require semi-elective mechanical ventilation to prevent re-
spiratory arrest. The principle problem in asthma is expiratory airflow limitation resulting in inspiration
before the previous breath has been fully exhaled. Consequently, the residuals of each breath are
‘stacked’ (Air trapping). Over time this will increase lung volume and chest wall expansion to the point
where further breaths are impossible.
Rapid sequence induction of anaesthesia, tracheal

intubation and ventilation in such a situation is extremely
hazardous BUT can be life-saving.
At the time ventilation is instituted the chest will already be near maximal expansion and it is imper-
ative that the practitioner’s focus is on preventing hypoxia and allowing expiration and NOT to aim
for normal SpO2 or EtCO2 by using large tidal volumes and a high respiratory rate. In the absence of
reversible causes such as pneumothorax, equipment failure or tube malpositioning, oxygen satura-
tions as low as 80% and end-tidal carbon dioxide as high as 80mmHg are compatible with life and
acceptable.
Tidal volumes should be kept low with expiratory pauses as long as possible. Ventilator circuit or BVM
should be disconnected during expiration and the practitioner should listen to the airflow emanating
from the tracheal tube. The next breath should only be provided when the expiratory flow has ceased
or saturation drops below 90%. Expiration can be aided by gently compressing the chest during expi-
ration.
Hand ventilation is preferable initially until the chest is sufficiently deflated to allow ‘normal’ tidal vol-
umes and a rate of 5 to 8 breaths should be set on the ventilator.
Hypotension is to be expected and should initially be managed with fluids and further reduction in
inspiratory pressures, followed by the use of a vasopressor.
In cardiac arrest due to asthma, bilateral chest

decompressions should be considered (for
CCPs only).
CPG 4.1
ADULT MEDICAL CARDIAC ARREST

MANAGEMENT
MANAGEMENT AIM
The aim of Cardiopulmonary Resuscitation (CPR) in adult medical cardiac arrest is to perform effec-
tive resuscitation that is likely to restore oxygen delivery and maintain circulation and perfusion of vital
organs to allow for return of spontaneous circulation (ROSC) and/or successful defibrillation. While
CPR and rapid defibrillation remain the standard first line of treatment for adult medical cardiac arrest,
successful resuscitation requires an integrated set of five coordinated events. These five interdepen-
dent events are represented by the links in a Chain of Survival, and include:
1. Immediate recognition of cardiac arrest

2. Prompt initiation and continuation of CPR
3. Early defibrillation
4. Timely advanced cardiac life support (ACLS); and
5. Early and appropriate post-cardiac arrest care.
At HMCAS CPR is defined as a treatment bundle that includes high quality CPR*, defibrillation and
airway and ventilatory support, as well as advanced cardiac life support (ACLS) drug management in
the form of Adrenaline/ Epinephrine and Amiodarone.
*Components of high quality CPR include:
Chest Compression Fraction (CCF) >80%
Minimal interruptions in CCF.
Chest Compressions Rate (CCR) of 100 to 120/min.
Chest Compression Depth (CCD) of at least one-third
of chest diameter.
Chest recoil: No residual leaning and allowing
for full chest recoil.
Avoiding ventilations at more than 10 per minute.
When a patient is in cardiac arrest, blood circulation stops. Soon afterwards the body starts to die.
Chest compressions and defibrillation are the only intervention that can get the heart pumping again.
During cardiac arrest, the stagnant arterial blood still contains unused oxygen reserves and will contin-
ue to do so for a short period of time. Circulating this stagnant blood with some oxygen to the vital or-
gans offers greater benefit than delaying compressions to first re-oxygenate blood. This is the reason
behind the change from ABC to CAB, with the focus being placed on compressions first.
Feeling for a pulse, opening the airway, clearing the airway, and providing ventilations are important
and lifesaving, however they delay the start of compressions.
NO MORE PULSE CHECKS TO DETECT CARDIAC ARREST.

The presence of agonal chest wall movements, agonal breaths, and clinical inexperience in determin-
ing the presence or absence of a pulse delays the start of compressions and decreases the chances
of ROSC.
There is no evidence that checking for a pulse is better than determined level of unconsciousness with
no breathing or no normal breathing to detect cardiac arrest.
There is a low risk of injuring a patient by starting CPR, in someone later found not to be in cardiac
arrest. The overall benefit of early CPR far outweighs any injuries that may be caused.
WHEN TO COMMENCE CPR?
STEP 1 - Determine if the victim is unconscious.
A person is considered unconscious if they do not answer, move or moan to a “shout and shake”. If a
patient is not awake and not moving, immediately tap or shake them on their shoulders and ask loudly,
“ARE YOU OK?” If the person is conscious they are likely to answer, move, or moan, if not the patient
is considered to be UNCONSCIOUS.
STEP 2 – Expose the patient’s chest.

As soon as a state of unconscious is determined – expose the patient’s chest so you can determine
if there is normal equal rise and fall of the chest. (Care should be taken to maintain patient privacy –
particularly in females).
STEP 3 - Assess for normal breathing.

Look at their exposed chest for at least 5 seconds but not more than 10 seconds. Normal breathing
is equal rise and fall of the chest. Do not try and determine the rate at this stage. If there is no rise
and fall of the chest, or gasps of air usually associated with a snore or grunting noise – this patient is
considered to have no normal breathing.
STEP 4 – Begin with compressions only.

If at any time during MANUAL compressions, the victim speaks out, moves, or moans, compressions
should be stopped immediately.
WHEN NOT COMMENCE CPR?

Undeniable Death
If the victim presents with evidence of undeniable death, any attempt at resuscitation is futile. You are
not obligated to initiate CPR in situations when death is undeniable. If in doubt, initiate resuscitation
while seeking consultation and advice from the CTL (Clinical Team Leader).
Criteria for undeniable death include: Decapitation, incineration, decomposition, rigor mortis, depen-
dent lividity, evisceration of major organs and fetal maceration.
Initial approach as per CPG 1: Clinical Approach to the Adult Medical Patient:
WITNESSED VERSUS UNWITNESSED ARREST
Arrest not witnessed by HMCAS staff with or Arrest witnessed by HMCAS staff with defibrillator
without bystander CPR attached
Unconscious Unconscious
No or no normal breathing No or no normal breathing
Perform chest compressions until pads applied Perform chest compressions until pads applied
Rhythm Analysis Rhythm Analysis
200J Shock given to VF/VT CCP- 3 stacked shock (200J, 300J, 360J) for VF/VT
Two minutes CPR AP – single shock (200J) for VF/VT
Rhythm Analysis-CHECK PULSE if organized rhythm Two minutes CPR
Rhythm Analysis-CHECK PULSE if organized

rhythm
CARDIAC ARREST MANAGEMENT
CPR INDUCED CONSCIOUSNESS
CPR induced consciousness occurs when chest compressions generate sufficient cerebral perfusion
pressure to make the patient conscious. These patients become unconscious when compressions are
stopped. If a patients LOC rises during compressions, stop compressions and confirm presence or
absence of ROSC. If no ROSC resume compressions immediately. If they awaken again they should
be sedated with Ketamine at 1mg/kg as a bolus dose.
REVERSIBLE CAUSES
Investigate for and treat reversible causes if found. Note that not all reversible causes can be treated
in the prehospital environment. If a reversible cause that cannot be treated in the field is identified,
consider initiating immediate transport to the hospital. Some of the causes which can be treated pre-
hospitally:
1. Hyperkalemia – consider Calcium Chloride. Hyperkalemia should be suspected in patients with:
renal failure (particularly if dialysis has been missed), drugs (e.g. angiotensin converting enzyme
inhibitors (ACE-I),angiotensin II receptor antagonists (ARB), potassium-sparing diuretics, non-ste-
roidal anti-inflammatory drugs, beta-blockers), or with tissue breakdown (crush injury or significant
burns > 48 hours prior).
2. Hypothermia – see CPG 10.2
3. Hypovolemia – Fluid Challenge, see CPG 4.7
4. Hypoxia – Ensure adequate oxygenation and ventilation
5. Tension Pneumothorax – Needle Decompression (CCP only, AP may perform needle
decompression under direct CCP supervision)
6. Toxins/Overdose – see CPG 8
CONDITIONS FOR CONSIDERING TERMINATION OF RESUSCITATION

Prolonged pre-hospital CPR that is clearly without any benefit may ONLY be terminated if the following
5 conditions are met (All 5 must be met):
1. 20 minutes of continuous Asystole despite ACLS CPR
2. Reversible causes treated
3. Cardiac arrest not from drug overdose and/or hypothermia
4. Family or patient’s significant other gives verbal consent (if family present)
5. Where no CCP on scene (in the case of APs). AP to confirm with CTL.
POST CARDIAC ARREST CARE
Pay particular attention to the following regarding post cardiac arrest care:
1. Airway and breathing: Aim to maintain a patient’s SpO2 > 90%. Do NOT hyperventilate the patient.
High EtCO2 is common post cardiac arrest.
2. Circulation: Maintain a systolic blood pressure (SBP) above 90mmHg. Using a combination of
250ml boluses and inotropes. Aim for a maximum of 1L normal saline and 2L in special
circumstances.
3. Glucose control: Hyperglycaemia after resuscitation can lead to poor neurological outcome. Post
cardiac arrest care correct hypoglycaemia (<4.0mmol/L) to within normal ranges (4-6.7mmol/L). If
RBS is <4mmol/L, administer 50ml bolus of 10% Dextrose. Repeat test after 10 minutes and con-
sider second bolus if RBS remains <4.0mmol/L. Avoid hyperglycaemia (>6.7mmol/L).
4. Agitated patient: Management will depend on the degree of agitation and context. Patients show-
ing signs of awareness but tolerating the LT may require Ketamine and possibly paralysis. Patients
demonstrating purposeful movements after a short period of resuscitation should be allowed to
recover, where those moving without purpose after prolonged resuscitation are unlikely to recov-
er fully and will benefit from neuroprotection (adequate oxygenation and ventilation, temperature
control).
The decision to exchange the LT for an ETT is at the discretion of the CCP and will depend on cir-
cumstances such as adequacy of LT airway, complexity of evacuation, distance to hospital, predicted
difficulty in intubation and hemodynamic status (haemodynamic instability may arise from the use of
drugs and of cardiovascular stimulation when intubating the trachea).
MOVING THE PATIENT:

1. Moving during CPR (even with the LUCAS II working) or for up to 10 minutes post-ROSC is not
recommended, as it can cause periods where the chest compressions become ineffective, or car-
diac arrest can reoccur, diminishing chance of survival. Where possible undertake all resuscitation
efforts on the scene. Consider moving the patient under the following circumstances:
 After a reasonable period of high quality CPR has been provided, without response to CPR and
the patient remains in VF/VT or PEA.
 If the family are demanding that the patient be moved and you are unable to convince them of
the benefit of continuing the resuscitation where you are
 If there are any hazards present which may endanger the staff or the patient
2. Try to limit the periods without chest compressions to a maximum of 10 seconds, trying to provide
a 2-minute cycle of chest compressions between patient movements.
3. Update CTL if you are moving the patient to hospital with on-going CPR, so they can pre-notify the
receiving facility.
CPG 4.2 MANAGEMENT OF ACUTE CORONARY SYNDROMES
TIME CRITICAL
CvPG TRANSPORT
4.2 ACUTE CORONARY SYNDROMES
Does the patient have a history of:  Pulmonary Embolism

 chest pain, hypertension, diabetes,  Oesophageal spasm
high cholesterol, smoker or ACS in  Aortic aneurysm
family?
 Pericarditis
 Type of pain/ Time of onset of pain?
 Chest Wall inflammation
 Pain changed by position?
 Aspirin 300mg orally (chewed and swallowed)

 GTN 0.4mg sublingually
 Acquire a 12-Lead ECG (confirm with CTL if patient must go to
Heart Hospital)
 Penthrox 3mls
 Clopidogrel 300mg (For AP only administer on advice of CTL)
 Fentanyl 1-2mcg/kg in 25-50mcg increments for pain control if

needed.
 Transport to Heart Hospital if the patient meet admission criteria
 Do not allow the patient to walk.

 If the patient has signs of Right Ventricular, Posterior or Inferior ACS,
use nitrates with caution – maintain SBP >90mmHg.
 Use fluid boluses (250ml - 500ml NS) to increase blood pressure if SBP
is < 90 mmHG.
AP & CCP CCP
CPG 4.2
TIME CRITICAL TRANSPORT
MANAGEMENT OF ACUTE CORONARY

SYNDROMES
MANAGEMENT AIM
To identify ACS early and triage and transport the patient to the most appropriate facility to facilitate
primary IV (fibrinolysis) or percutaneous coronary intervention (PCI) thus limiting myocardial damage.
The clinical indicators which suggest the AIM is being achieved are the following:
1. Maintain SpO2 levels (≥ 95%) and decrease patient dyspnoea if present.
2. Early 12-Lead ECG triage
3. Early oral anti-platelet therapy
4. Early GTN administration
5. Early pain control using oral, inhalational or IV analgesics to achieve pain scale less than 4/10 or
3rd face (CPG 6.1 pain management)
6. Transportation to most appropriate facility (Heart Hospital) with pre-arrival notification.
7. Limiting on-scene time without compromising safety or patient care.
RECOMMENDED TREATMENT:
2. Important considerations:
 Calm and reassure the patient and family to reduce patient anxiety and thus reduce myocardial
oxygen demand.
 Administer oxygen as per CPG 3.3 only if patient is hypoxemic (SpO2 < 95%), cyanotic or there
is evidence of heart failure with pulmonary oedema. Supplemental oxygen should not be ad-
ministered to patients with a SpO2 ≥ 95% in the presence of ACS, as it may worsen outcomes.
3. Administer oral aspirin to be chewed and swallowed. Withhold if contraindicated or the patient has
a true allergy (risk of life-threatening anaphylactic reaction).
4. Administer sublingual GTN at approximately 5-minute intervals for initial pain management, unless
contraindicated.
5. Acquire a 12-Lead ECG as early as possible on any patient suspected of ACS with active chest
pain, unexplained nausea and vomiting, dizziness or shortness of breath. Interpretation of the
12-Lead and triage to Heart Hospital must be undertaken by a CCP (CTL via telemetry or CCP on
scene). Leave 12-Lead cables on patient until care is transferred. DO NOT DELAY administration
of aspirin to obtain 12-Lead ECG.
6. Administer oral Clopidogrel to be swallowed (AP staff – with CTL permission only). Withhold if con-
traindicated (may still be administered if the patient has an allergy to aspirin).
7. If effective analgesia is not achieved with GTN, consider:
 Inhaled Penthrox (APs and CCPs) and/ or
 IV Fentanyl (CCP, continuous monitoring of ECG and SpO2 required)
 IV Paracetamol is not indicated for the management of ischemic cardiac pain.
 If GTN causes a drop in BP, manage with small fluid boluses (250ml and reassess) to increase
SBP > 90mmHg.
 If the patient becomes acutely unstable, manage any underlying bradycardia as per CPG 4.5.1,
or shock as per CPG 4.7 after an initial attempt at fluid therapy.
CPG 4.2 ACS 12-LEAD ECG DECISION TREE
This algorithm provides a guideline to assist in identifying patients at greatest risk for
Acute Coronary Syndrome and who require a 12-Lead ECG
Initial history, clinical presentation and vital signs
Age ≥ 30 with: Age ≥ 50 with: Age ≥ 60 with: Age ≥ 70 with:
 Chest pain  Dyspnea  Hx of Diabetes  Abdominal pain

 Palpitations  Decreased GCS  Female patient  Nausea/ Vomiting
 Upper extremity pain
 Syncope
 Weakness
12 Lead ECG 12 Lead ECG 12 Lead ECG 12 Lead ECG

recommended recommended recommended recommended
Use clinical judgement to

determine need for 12-Lead ECG
***MEETS ST ELEVATION MI CRITERIA***
Initiate treatment Update CTL with Minimise time on Meet Charlie Unit
as per CPG 4.2 patient details scene. Load patient en-route if required
to notify Heart and transport as soon
Hospital as possible
CPG 4.3 MANAGEMENT OF ACUTE PULMONARY OEDEMA
CPG 4.3 PAGE 60

HMCAS CLINICAL PRACTICE GUIDELINES Version 1.4 2019 BACK TO TABLE OF CONTENTS
CPG 4.3
MANAGEMENT OF ACUTE PULMONARY

OEDEMA
MANAGEMENT AIM
To Improve oxygenation by reducing pulmonary congestion and increasing the FiO2 (percentage of
oxygen inspired). The clinical indicators which suggest the AIM is being achieved are the following:
1. Maintain SpO2 level ≥ 95%
2. Reduce pulmonary congestion and associated work of breathing
3. Reduce preload and afterload or increase cardiac output if hypotension present.
4. Promote diuresis if evidence of fluid overload present
5. Acquire 12-Lead ECG if potential for ACS present
6. Transport to the most appropriate facility with pre-arrival notification.
1. Initial assessment: undertake a rapid assessment of the history (specifically of chronic hyperten-
sion and medication, previous episodes of breathlessness, breathlessness at night (paroxysmal
nocturnal dyspnoea) or on lying down (orthopnoea) and effort intolerance (breathless on exertion).
2. Assess the respiratory function including assessment of lung sounds front and back. Assess
ankles, abdomen and neck for signs of fluid overload. The blood pressure is a key indicator as to
the drug therapy regime to be utilised in managing these patients, thus ensure an accurate reading
(repeat automated BP or do manual BP as confirmation).
CPG 4.3 PAGE 61

2. Oxygen therapy aim is to increase the patients SpO2 ≥95%. Work with the patient to select a meth-
od most comfortable for the patient that achieves adequate oxygenation. If the patient will tolerate
it change to Continuous Positive Airway Pressure (CPAP-CPG 3.4) as the method of choice.
CCP therapy for APO is focused on increasing

oxygenation using CPAP (CPG 3.4) and reducing
pulmonary congestion using GTN.
3. For patients with normal to high BP and APO, manage with early and high dose sublingual GTN and
CPAP. Administer ongoing GTN via intravenous infusion.
4. If hypotension is present (SBP < 90mmHg), consider initiating IV inotropic support (Adrenaline/Epinephrine)
to improve cardiac output. Inotropes should only be used in the presence of heart failure with hypotension.
See guidelines on non-traumatic / cardiogenic shock (CPG 4.7).
5. Acquire a 12-Lead ECG on all patients with active chest pain suspected to be cardiac in origin.
Interpretation of the 12-Lead and triage to Heart Hospital must be undertaken by a CCP (CTL via
telemetry or CCP on scene) to save time.
CPG 4.3 PAGE 62

CPG 4.4 MANAGEMENT OF ADULT SEPSIS
4 TIME CRITICAL INTERVENTION
.4 Assessment Reminders
Early recognition by Quick Sequential Organ Failure Assessment (qSOFA):
 Altered mental status (GCS < 15)
 SBP≤ 100mmHg
 RR ≥ 22bpm
Suspected Sepsis?
 Provide High flow O2/attach nasal ETCO2
 Establish IV/IO access
 Administer 500ml NS fluid bolus to achieve
SBP≥90mmHg and/or MAP≥65mmHg
 Repeat 250-500ml NS bolus if required and if
no signs of fluid overload present (Max 2L)
If no response to fluid challenge, provide

pharmacological support.
SEPTIC SHOCK
 Noradrenaline infusion 0.01-0.3mg/kg/min
 Titrate to effect
 Target MAP ≥ 65mmHg/SBP≥90mmHg
Monitor patient closely and transport to closest

appropriate facility with pre-notification if
possible.
NOTE:
 The most common presenting symptom in sepsis is tachypnoea.
 Monitor for signs of fluid overload.
 Sepsis should be suspected in the generally unwell immunosuppressed patient.
 Whilst fever is commonly associated with sepsis, hypothermia is usually associated with a higher
morbidity, especially in the elderly.
AP & CCP CCP
CPG 4.4
MANAGEMENT OF ADULT
SEPSIS
MANAGEMENT AIM
Sepsis is defined as life threatening organ dysfunction caused by a dysregulated host response to
infection. Management of these patients requires prompt recognition, immediate treatment and timely
transport to an appropriate facility.
qSOFA:
 Altered mental status GCS < 15

 SBP ≤ 100mmHg
 RR ≥ 22 bpm
1. Initial approach as per CPG 1: Clinical Approach to the Adult Medical Patient
2. Prehospital sepsis management requires:
 Early identification
 Early oxygenation
 Early haemodynamic resuscitation
 Hospital pre-notification (if possible)
3. Initiate oxygen therapy as per CPG 3.3. Consider if CPAP needed. Maintain and protect airway
if required.
4. Administer fluid bolus of 500ml NS to maintain SBP>90mmHg and/or MAP>65mmHg. Repeat
250-500ml fluid bolus as required if no signs of fluid overload present, up to a maximum of 2L.
5. Assess response to fluid challenge as this will guide further treatment and triage the
patient into fluid responsive or non-fluid responsive shock.
6. If no response to fluids provide pharmacological support.
 Noradrenaline 0.03-0.1mcg/kg/minute
 NB: If administering emergency infusion through peripheral IV, ensure that IV is well placed
(Forearm preferred site, if using ACF, splint arm to prevent flexion) and free flowing. 18G
preferred size cannula. Monitor closely for extravasation. If extravasation occurs, stop
infusion immediately and disconnect. Gently aspirate extravasated solution (do NOT flush
the line); remove needle/cannula; elevate extremity. Report extravasation to ED staff on hand-
over.
7. Monitor the patient closely and transport to closest appropriate facility with pre-notification.
CPG 4.5.1 MANAGEMENT OF ADULT SYMPTOMATIC
BRADYARRHYTHMIAS
 Patient symptomatic?  Drug overdose (Bblockers, Calcium

 Decreasing LOC channel blockers)
 Hypotension  Hypothermia
 Signs of shock and dizziness  Raised ICP
 Acute Coronary Syndrome
 For bradyarrhythmias:
 Atropine 0.5mg IV (repeat up to maximum of 3mg)
 External cardiac (transthoracic) pacing: start at 30mA and 70bpm – increase
mA as required to the maximum allowed by the device.
 For bradyarrhythmias associated with ACS:

 Consider external cardiac (transthoracic) pacing
 If Atropine and pacing fails to improve BP:

 Adrenaline/ Epinephrine IV/IO infusion: mix 2mg 1:1000 with 18ml NS in
20cc syringe – start at 2ml/hr (3.3mcg/min), double if required
 Rule out other causes of bradyarrhythmia before undertaking above

interventions
 If patient has signs of inferior ACS – initiate managment of bradyarrhythmia
if patient becoming significantly unstable
AP & CCP CCP
HMCAS CLINICALPRACTICE GUIDELINES Version 1.4 2019 CPG 4.5.1 PAGE 65

CPG 4.5.1
MANAGEMENT OF ADULT
SYMPTOMATIC BRADYARRHYTHMIAS
MANAGEMENT AIM
To recognize symptomatic or immediately life threatening bradyarrhythmias and to utilise non-pharma-

cological, pharmacological or electrical intervention to terminate or modify the arrhythmia. The clinical
indicators which suggest the AIM is being achieved are the following:
1. Recognise the signs and symptoms of a life-threatening bradyarrhythmia including: breathless-
ness, chest pain, hypotension and/or decreasing level of consciousness.
2. Determine if the bradyarrhythmia is symptomatic or immediately life-threatening and apply the
appropriate intervention.
3. Symptomatic bradyarrhythmia is managed in an escalating manner.
4. The immediately life-threatening bradyarrhythmia is managed by electrical intervention (pacing).
5. Termination or modification of the bradyarrhythmia produces an improvement in clinical condition.
1. A bradyarrhythmia may reduce cardiac output causing reduced forward flow and end organ perfu-
sion with onset of dysfunction (hypotension, decreased level of consciousness, clinical shock and
dizziness).
2. Undertake a rapid assessment of the history (specifically of previous episodes, medications, timing
of onset of arrhythmia in relation to chief complaint) and of precipitating factors (chest pain, dizzi-
ness, exercise intolerance).
2. If required, initiate oxygen therapy as per CPG 3.3. Avoid high pressures with Continuous Positive
Airway Pressure (CPAP) as these may further reduce cardiac output worsening the patient’s condi-
tion. The aim of supplemental oxygenation is to increase the patient’s SpO2 ≥ 95%. Based on a
4-Lead ECG diagnosis AND patient’s clinical condition:
3. For symptomatic bradycardia (sinus bradycardia or conduction block with 2nd degree Mobitz or
3rd degree AV block, with signs of end organ dysfunction:
 Consider administering Atropine (use with caution if associated with ACS – use only in a rapidly
deteriorating patient),
 And/or transthoracic pacing
 And/or an inotropic infusion using Adrenaline/ Epinephrine.
4. Acquire a 12-Lead ECG on all patients with arrhythmias where possible. Do not delay lifesaving
intervention to acquire the 12-Lead ECG
5. If pacing considered then start at a rate of 70bpm and 30mA, increasing the energy until elec-
trical and mechanical capture are noted (to maximum energy allowed by device as required).
If no improvement in blood pressure following capture, increase the rate up to a maximum of
80 - 90bpm. If pacing fails to improve the blood pressure, consider adding inotrope as above.
6. Provide pain relief during pacing as required (see CPG 6.3 Safe sedation and monitoring in
Adults)
7. If the specific cause of the bradycardia is known, treat the cause early if possible.
 Hypoxia – CPG 3.3
 Hypothermia – CPG 10.2
 Drug Overdose or Ingestion – CPG 8
 Hyperkalemia – Consider Calcium Chloride
CPG 4.5.2 MANAGEMENT OF ADULT SYMPTOMATIC TACHYARRHYTHMIAS
 Patient symptomatic?  Hypoxia

 Decreasing LOC  Hyperthermia/ fever
 Hypotension/ dizziness  Hypoglycaemia
 Shortness of breath  Hypovolaemia (shock)
 Attempt Valsalva (Blow on 10ml syringe for 15 seconds)
Narrow Complex Tachyarrhythmia – SVT

 Immediately life-threatening: Synchronised cardioversion 100J
 Symptomatic:
 Adenosine 6mg IV with flush, single repeat 12mg IV with flush
 Amiodarone 300mg IV over 10 –15 minutes
Narrow Complex Tachyarrhythmia – AF or Atrial Flutter

 Symptomatic: Amiodarone 300mg IV over 10 - 15 minutes. Avoid
conversion of AF if symptoms greater than 48 hours, unless it is
life-threatening. NB: rule out non-cardiac causes first!
Wide Complex Tachyarrhythmia

(perform unsynchronised shock if sync is not successful – irregu-
lar wide complex/ polymorphic VT)
 Symptomatic:
 Amiodarone 300mg over 15 minutes (monomorphic VT)
 Magnesium 2g over 15 minutes (Torsades de Pointes ONLY)
 Cardioversion energies may be escalated if first shock unsuccessful.

 Conversion of AF that is > 48 hours old carries risk of embolic event,
avoid unless condition is life threatening.
AP & CCP CCP
HMCAS CLINICALPRACTICE GUIDELINES Version 1.4 2019 CPG 4.5.2 PAGE 68

CPG 4.5.2
MANAGEMENT OF ADULT
SYMPTOMATIC TACHYARRHYTHMIAS
MANAGEMENT AIM
To recognize symptomatic or immediately life-threatening tachyarrhythmias and then utilise non-phar-

macological, pharmacological or electrical intervention to terminate or modify the arrhythmia. The
clinical indicators which suggest the aim is being achieved are the following:
1. Recognise the signs and symptoms of a life-threatening tachyarrhythmia including: breathless-
ness, chest pain, hypotension or decreasing level of consciousness.
2. Determine if the tachyarrhythmia is symptomatic or immediately life-threatening and apply the
appropriate intervention.
3. The symptomatic tachyarrhythmia is managed in an escalating manner.
4. The immediately life-threatening tachyarrhythmia is managed by electrical intervention (synchro-
nized cardioversion).
5. Termination or modification of the tachyarrhythmia produces an improvement in clinical condition.
1. A tachyarrhythmia may reduce cardiac output causing reduced forward flow and end organ perfu-
sion with onset of dysfunction (hypotension, decreased level of consciousness, clinical shock and
dizziness). Increasing build-up of atrial pressure produces pulmonary congestion and the rapid
rate (in tachyarrhythmias) reduces coronary flow producing myocardial ischemia and chest pain.
2. Undertake a rapid assessment of the history (specifically of previous episodes, medications, timing
of onset of arrhythmia in relation to chief complaint) and of precipitating factors (chest pain, drugs,
alcohol, caffeine, dizziness, exercise intolerance).
2. If required initiate oxygen therapy as per CPG 3.3. Avoid high pressures with Continuous Positive
tion.
3. Establishing an IV line for drug access and fluid therapy as required
4. Based on the 4-lead ECG diagnosis AND patients clinical condition:
5. If the ECG demonstrates a tachyarrhythmia and signs of end organ dysfunction are present: de-
termine if this is a primary tachyarrhythmia or the result of a physiological response (hypotension,
hypoxia, hypoglycaemia, fever etc). In rates over 150, primary tachyarrhythmia is more likely the
cause of the end organ dysfunction, as opposed to a physiological response. Maximum physiolog-
ical response is age dependent (220 bpm minus age) and can be used to assess the likelihood of
the arrhythmia being physiological or pathological
6. In unstable tachyarrhythmias (wide [>0.12sec] or regular / irregular narrow complex) with signs of
imminent death (severe hypotension, decreasing GCS and/or severe pulmonary oedema) immedi-
ate synchronized cardioversion is advocated using the following energy settings:
 Wide complex regular [monomorphic VT] - 200J biphasic,
 Wide complex irregular [polymorphic VT] – 200J biphasic unsynchronized shock (if monitor will
not synchronise)
 AF 200J biphasic,
 Narrow complex 100J biphasic
Synchronized cardioversion is dependent on the monitor

being able to identify an R wave. If the rhythm is wide and
irregular, such as in polymorphic VT, the monitor may not
be able to identify a regular R wave and will not synchronize
and will not deliver a shock. If synchronization fails change
the lead being monitored and adjust amplitude. In the
presence of life threatening tachyarrythmia, if the monitor
cannot synchronize to the ECG, standard defibrillation
(unsynchronized) should be performed.
Consider repeating with an escalated energy setting if
there is no response to the first shock. Sedation should be
considered before cardioversion (If sedation is used, caution
must be exercised. Minimal dose should be applied to
prevent worsening of hypotension)
7. For symptomatic narrow complex tachyarrhythmias (with moderate end organ dysfunction – dizzi-
ness, palpitations, mild chest pain, borderline hypotension or mild to moderate SOB without frank
pulmonary oedema):
 Regular tachyarrhythmias (SVT/ PSVT/ AVRT/ AVNRT) require rhythm control to reduce
end-organ dysfunction.
» Attempt vagal manoeuvres (i.e. valsalva manoeuver – ask patient to try blow plunger out of
a 10 ml syringe for 15 seconds) while preparing the recommended doses of Adenosine.
» Use a double syringe technique (Adenosine + Saline flush) and a rapid IV push of both
syringes for the administration of the Adenosine.
» If no response to the repeated Adenosine dose, rule out other causes for tachyarrhythmia
and administer Amiodarone 300mg IV infusion over 10-15 minutes.
 The management of Atrial Fibrillation with rapid ventricular response (fast ventricular rate with
onset of symptoms) requires rate control of the arrhythmia.
» Reduce the rate of the AF with Amiodarone. Adenosine must be avoided in AF as potential
underlying accessory pathways may precipitate VF if the AV node is blocked. Amiodarone
should be used with caution if onset > 48hrs or unknown as it may convert the rhythm to
sinus with risk of embolisation. Use only if symptomatic tachycardia.
»NB: Identify potential non-cardiac causes of AF (e.g. sepsis, hypoxia) prior to administering
Amiodarone and manage appropriately. Amiodarone IS NOT for routine management of
AF unless the AF is of cardiac origin, symptomatic requiring rate control and is <48 hours
onset. If AF of a non-cardiac origin, manage according to relevant CPG (e.g. fluids,
oxygen, analgesia).
 For symptomatic but not life-threatening wide-complex tachyarrhythmias:
» In ventricular origin (QRS wider than 140ms) tachyarrhythmias: differentiate between
monomorphic or polymorphic VT (Torsades de Pointes). Administer Amiodarone to mono-
morphic VT and Magnesium to polymorphic VT.
8. Do a 12-Lead ECG on all patients with tachyarrhythmias where possible. Do not delay life-saving
intervention to acquire the 12-Lead ECG.
CPG 4.6

CPG 4.6
MANAGEMENT OF PULMONARY
EMBOLISM
MANAGEMENT AIM
To recognize a life-threatening pulmonary embolism and utilise interventions to attempt to limit the
progress of hypoxemia and shock. The clinical indicators which suggest the AIM is being achieved are
the following:
1. Recognise clinical signs of a large pulmonary embolism.
2. Where hypoxia and shock cannot be reversed provide immediately life preserving interventions
and transport to an appropriate facility with pre-notification.
The most sensitive clinical indicators of PE are a combination of dyspnoea or tachypnoea (RR > 20)
with pleuritic chest pain and signs of deep vein thrombosis (DVT).
2. Establish an airway if the patient has a decreased level of consciousness. RSI (CPG 2.3) to pro-
tect the airway and provide mechanical ventilation (CPG 3.4) is extremely hazardous and cardiac
arrest is highly likely on induction and should be avoided. CPAP can be considered.
3. If required initiate oxygen therapy as per CPG 3.3. The aim of supplemental oxygenation is to
increase the patient’s SpO2 ≥95%. In large PE the SpO2 may not rise which may be a clue to the
diagnosis.
4. Consider establishing an IV line for drug access and fluid therapy as required
5. In the presence of shock (SBP< 90mmHg) administer fluid boluses – 250ml NS (repeat a second
time) to increase the SBP >100mmHg. If the patient’s condition does not respond to fluids adminis-
ter a Phenylephrine infusion to increase BP.
6. Administer analgesia (CPG 6.1) cautiously as required remembering opioids may further reduce
blood pressure.
CPG 4.7
CPG 4.7
MANAGEMENT OF NON-TRAUMATIC
SHOCK
MANAGEMENT AIM
To recognize life-threatening shock and then utilise either non-pharmacological or pharmacologi-

cal interventions to halt or slow down the progress of the shock while transporting the patient to an
appropriate facility for definitive management. The clinical indicators which suggest the AIM is being
achieved are the following:
1. Recognise clinical signs and symptoms of shock and identify (where possible) the cause. (Use
SBP<90mmHg or MAP 70-80mmHg as a guideline).
2. Determine if the cause of shock can be reversed and implement the appropriate intervention.
3. Where the progression of shock cannot be reversed, provide immediately life saving interventions
and then transport to an appropriate facility with pre-notification.
NON-TRAUMATIC SHOCK TYPES
Hypovolemic Caused by dehydration due to vomiting, exposure to high temperatures and

reduced fluid intake.
Cardiogenic Caused by left or right ventricular failure. Hypotension is associated with

poor peripheral perfusion and pulmonary congestion. The patient may have
a history of heart failure or AMI (past or present). Signs of vascular conges-
tion help in the diagnosis (raised JVP and peripheral oedema.)
Obstructive Severe life-threatening bronchospasm or airway obstruction with significant

air trapping causes increased intrathoracic pressure and compression of
the heart reducing venous return and thus cardiac output.
Septic Caused by significant infection and is often associated with fever. In the
initial stages pulse and blood pressure may be normal or bounding (high
output failure) with a late cardiovascular collapse.
Anaphylactic Shock associated with severe allergic response with signs and symptoms
of rashes, hives, wheezing and angio-oedema of a body parts or the airway.
2. Establish an airway if the patient has a decreased level of consciousness. Consider RSI (CPG 2.3)
to protect the airway. Caution must be exercised with the selection and dose of induction agent as
this may worsen the degree of shock.
3. If required initiate oxygen therapy as per CPG 3.3. Avoid high pressures with Continuous Positive
tion.
4. Based on the cause of shock AND patient’s clinical condition:
 Hypovolemic Shock
» Administer NS in 500ml boluses to max of 2,000ml if no signs of pulmonary edema
 Cardiogenic Shock
» Administer 250-500ml NS bolus.
» Repeat NS bolus if continued signs of shock to a max of 1,000ml if no signs of pulmonary
oedema.
» If continued signs of shock or pulmonary oedema present initiate Noradrenaline infusion.
 Septic Shock: Treat as per CPG 4.4
 Anaphylactic Shock: Treat as per CPG 2.2.1
5. Large fluid volumes should be avoided in the elderly, patients with renal failure and/or in cardio-
genic shock.
6. Assess the responsiveness to fluid challenges as this will guide further treatment and triage of the
patient into fluid-responsive or non-fluid responsive shock.
7. Initiate specific interventions according to HMC clinical practice guidelines where a definite cause
is identified (ie ACS, Pulmonary embolism or anaphylaxis).
8. Monitor the patient carefully especially level of consciousness.
CPG 5.1 MANAGEMENT CEREBROVASCULAR ACCIDENT / STROKE
 Face: Facial droop?  Intoxication

 Arms: Unilateral weakness?  Hypoxia
 Speech: Slurs words or has difficulty  Hypoglycaemia
speaking  Seizures
 Time: Document time last seen normal  Cerebral Infections
or time of symptom onset
 Migraine
 Position lateral
 Positive FAST:
 Onset Time < 8 hours OR wake-up Stroke (Patients who wake up from
sleep with symptoms of Stroke) – Priority 1 to HGH (with pre-notification
via CTL)
 Onset Time > 8 hours – Priority 2 to HGH
 Manage en route
 If patient unconscious with airway compromise consider RSI
 Time is based on when patient was last seen normal or when symptom
started - Document as accurate as possible.
 DO NOT delay transport to wait for CCP.
 Pre-notification important so Bay 1, Stroke team and CT scan can be pre-
pared.
 All suspected Stroke patients should be transported to HGH regardless of
onset time
AP & CCP CCP
CPG 5.1
MANAGEMENT OF STROKE
MANAGEMENT AIM
To identify CVA, triage the patient to an appropriate facility while providing life support care en route.
1. Identify CVA utilizing the FAST system.
2. Manage any associated immediately life threatening conditions en route.
3. Provide pre-notification of the receiving facility, via the CTL, as early as possible.
4. Provide urgent (P1) transportation to HGH-ED Bay 1 to those patients whose symptom-onset fit
into the 8-hour window or who wake up from sleep with symptoms of stroke.
When assessing a patient with potential for CVA consider and rule out the following conditions which
can mimic CVA:
 Intoxication – Alcohol/ Drugs
 Hypoxia
 Hypo/ hyperglycaemia
 Seizures
 Syncope/ fainting
 Cerebral infections (meningitis, encephalitis)
 Middle Ear disorder (history of ear pain in the last few days, with severe dizziness)
 Migraine (photophobia)
STROKE ASSESSMENT TABLE
Normal Abnormal
Face Patient shows teeth or Both sides of face One side of the face
smiles move equally does not move as well as
the other side.
Arms Patient lifts both arms Equal arm raise or Unable to lift one arm or
or squeezes with both grip strength unilateral weakness in
hands one arm.
Speech Patient able to talk Talks clearly without Slur words, says the
clearly slurring wrong words or is unable
to speak or understand
commands.
Time Time last seen normal or time from symptom onset
2. Place the patient in a lateral position if the patient has a decreased level of consciousness. Con-
sider RSI (CPG 2.3) to protect the airway. The need for RSI and ventilation is a sign the patient is
in extremis. Do not delay transport.
3. Do not use oxygen unless the patient is hypoxic or exhibits shortness of breath (as per CPG 3.3).
4. Conduct an RBS test to rule out hypo/ hyperglycaemia. This should be done en route to minimise
scene time and/ or delays in transportation to hospital.
5. If the FAST test is positive and onset of symptoms is less than or equal to 8 hours or for patients
who wake up from sleep with symptoms of Stroke, transport the patient Priority 1 to HGH Bay 1
with pre-notification. If symptoms are new to the patient but are more than 8 hours from onset and
they did not wake up with the new symptoms, transport Priority 2 to HGH. If the onset was not
witnessed, the time the person was last seen normal must be used.
6. Where possible, establish peripheral IV access en route to minimise scene time and/ or delays in
transportation to hospital.
7. Transport the patient in a lateral or semi-fowlers position depending on level of consciousness.
8. Given the time-sensitive nature of these patients, be prepared to take the patient directly to CT
Scan unit via Bay 1 to reduce door to needle time for those patients requiring thrombolysis.
If you require CCP assistance,
DO NOT WAIT ON SCENE FOR CCP.
If patient is within the 8-hour window or woke up with
symptoms of Stroke, meet the CCP en route.
CPG 5.2 MANAGEMENT OF ADULT SEIZURES
 Is the area around the patient safe?  Hypoxia

 Rule out reversible causes  Hypoglycaemia
 Past history of seizure?  Stroke
 Focal or generalised seizures  Severe anxiety reactions
 Rule out reversible causes

 Provide oxygen if seizures prolonged (> 5 minutes)
 Midazolam:
 IN: 0.2mg/kg (max 1ml / nostril / dose)
 IM: 0.2mg/kg – up to maximum of 10mg per injection, repeat after 15
minutes if required
 IV/IO: 0.1mg/kg in increments of 5mg, up to maximum of 20mg.
 The IN route is first line and preferred if no IV in situ. The second line is IM.
 Only administer Midazolam for prolonged (> 5 minutes) or recurrent seizures
(status epilepticus)
 Consider RSI (for patients 14 years and older) if seizures persist despite ade-
quate administration of Midazolam.
AP & CCP CCP
CPG 5.2
MANAGEMENT OF ADULT SEIZURES
MANAGEMENT AIM
To recognise seizures and initiate anticonvulsant therapy if required to prevent cerebral and other end
organ damage. The clinical indicators which suggest the AIM is being achieved are the following:
1. Recognising seizures and eliminating possible causes.
2. Early administration of appropriate anti-convulsant therapy.
3. Post-convulsion management to prevent further seizures.
1. Seizures are classified by their appearance and the effect it has on the patient’s level of conscious-
ness:
 Partial seizures affect only one part of the body producing motor, sensory, autonomic or psychi-
atric signs.
 Generalised seizures affect the whole body producing spastic (tonic) contractions, jerking
movements (tonic-clonic) or loss of motor function (atonic).
2. Generalized motor seizures involve the whole body. Status Epilepsy is defined as seizures that oc-
cur repeatedly without the patient regaining consciousness between each seizure. Status Epilepsy
may cause hypoglycaemia, hyperthermia and hypoxia, which may cause or worsen brain injury
leading to death. Urgent termination of the seizures is thus a priority.
2. In patients with active seizures basic airway management should be attempted and BVM ventila-
tion should be considered to prevent hypoxia due to spasm of the respiratory muscles.
3. In Status Epilepticus: administer Midazolam (IV, intranasal, IM or IO) – repeat dose after 5 minutes
if seizures persist. If this fails to terminate the seizures then an anaesthetic dose of Midazolam
should be used (0.2mg/kg). If the seizures persist despite benzodiazepine therapy consider RSI of
the patient (as per CPG 2.3).
 In pregnant female patients consider Magnesium therapy if the seizures are potentially due to
eclampsia (> 20 weeks gestation with history of hypertension or pre-eclampsia) – see eclamp-
sia (CPG 12.2) guideline.
 Use active external cooling methods if the seizures are associated with hyperthermia.
4. The patient in the post-ictal phase should be placed in the lateral position and monitored for vomit-
ing. Suction the airway as required (there may be excessive salivation following seizures).
5. If the patient receives sedation (eg midazolam) continuous ECG and SpO2 and ETCO2 monitoring
is required as soon as it can be applied. Other vital signs assessment as indicated in CPG 1. It is
understood that post ictal patients are often not compliant with monitoring and vital signs assess-
ments, try to calm and reassure the patient and reattempt vital sign observations. Visual confirma-
tion of the patient’s respiratory status and signs of perfusion are expected at all times.
CPG 6.1
MANAGEMENT OF PAIN
MANAGEMENT AIM
To interpret signs and symptoms of pain and implement effective control of pain. The clinical indicators
which suggest the AIM is being achieved are the following:
1. Recognise signs and causes of pain in the patient.
2. Initiate pain management to prevent suffering and clinical deterioration.
3. Re-evaluate pain score after pain therapy to ensure successful management of the pain.
1. Of all symptoms, pain cannot be objectively measured. It depends on gender, cultural background,
environmental and social factors as well as previous experience of pain.
Pain scoring: The following elements should be measured:
 Onset (how and when did it start?)
 What provokes the pain (what relieves or exacerbates the pain?)
 Quality (sharp, burning, dull, increasing)
 Radiation
 Site
 Timing of the pain
2. All patients should have a pain score assessment carried out.
3. Both the absolute value of the score as well as the patient’s own assessment should be used to
determine the type of analgesia and the route of administration that is most appropriate for the
circumstance.
4. The score should be repeated after pain management therapy. Reduction of pre-analgesia pain
score indicates effectiveness of intervention.
5. The trend of the score is the most important factor in assessing the efficacy of pain relief treat-
ment.
6. HMC Policy CL6078 on Pain screening, assessment and management includes various pain
scales of which some are applicable to EMS practice.
Adult pain scoring can be done using the visual analogue scale or the numeric rating scale
Pain relief intervention should be introduced in an incremental manner. Any pain relief decisions
should be taken in partnership with the patient. Consideration should be given to patients who are re-
ceiving chronic pain relief medications, as they may experience breakthrough pain despite their usual
medication regimen. They may require large doses of analgesics to have significant clinical effect.
Many conditions cause pain and treating the cause is an important aspect in attaining effective pain
relief (e.g. managing cardiac pain with GTN.) The following elements of pain relief treatment should be
considered at all times: timeliness, effectiveness and potential side effects.
TREATING THE PAIN
1. Non-pharmacological treatments
 Reassurance – fear and anxiety worsen the pain experience; explanation and reassurance may
aid with the treatment of pain.
 Splinting – splinting of fractures may aid relief of pain as well as minimises further trauma and
bleeding.
 Dressings – burn dressings aid further cooling the burn area and alleviate pain via this mecha-
nism. Care should be taken not to cool burns for more than 20 minutes and prevent the devel-
opment of hypothermia in large surface area burns.
2. Pharmacological treatments:
 Analgesic medications should be used in accordance with the drug formulary, considering the
assessment of indications and contraindications prior to the administration of any medication:
» Inhalational analgesics (Methoxyflurane - Penthrox) – Inhalational analgesia should be
considered as first line (if the patient is compliant and the pulmonary route is available).
However, it may be apparent from initial assessment that stronger analgesia may be more
appropriate to start with. Inhalational analgesia should be supplied until the enteral or
parenteral analgesics have had time to take effect. This form of analgesia can be used for
most causes of pain including cardiac and obstetric patients. AP/CCP
» Oral analgesics – Paracetamol and non-steroidal anti-inflammatory agents (Ibuprofen) can
be used in isolation or combination in pain. Care should be applied in cases of history of
gastric ulcerations and asthma in the case of NSAIDs. AP/CCP
» Parenteral analgesics –
 Effective pain relief often requires a multi-modal approach. Analgesia can be achieved
will lower doses of multiple drugs. Eg: the combination of inhaled methoxyflurane with
IV Paracetamol and Fentanyl for traumatic pain.
 IM/IV anti-inflammatory agent (Ketoralac or Diclofenac): this should be used in patients
with inflammatory induced pain, renal colic and inflammatory pain such as mechanical
back pain. Consider hydration status as these medications may produce renal toxicity.
Never administer both Ketoralac or Diclofenac to the same patient. [AP/CCP]
 IV Paracetamol – is an appropriate option for patients with moderate pain and can be
used in conjunction with Methoxyflurane and/or Fentanyl. IV Paracetamol has a
lesser side effect profile with no sedatory properties. It is as effective as morphine in
moderate traumatic pain and can also be used in obstetric pain. [CCP/ AP for adults;
CCP only for paediatrics]
 Fentanyl – Fentanyl is administered until a sufficient level of pain relief has been
achieved (pain score reduction of at least 50%). When administering Fentanyl,
Naloxone must be available at all times. Due to Fentanyl’s relatively short duration of
action, repeat doses may be required.
 Low dose Midazolam can aid in attaining relief where pain is associated with a high
degree of anxiety. Remember Midazolam has no analgesic properties, so use a
combination therapy.
 Ketamine is particularly useful in cases of trauma and burns as it does not cause
significant cardiovascular or respiratory depression. It is useful for “conscious sedation”
(see CPG 6.3) – providing analgesia and dissociation but allowing the patient to still be
alert enough to answer questions.
 If significant sedation and respiratory depression occurs due to the use of Fentanyl,
initially attempt to rouse patient using manual stimuli and instruct patient to breathe. This
may have to be repeated. The decision to reverse the opioid analgesia effects should be
carried out cautiously and incrementally.
NOTE: Specific drug doses should be given as per specific CPG.
MONITORING REQUIREMENTS
Certain medications for the management of pain such as Fentanyl, Midazolam and Ketamine can
result in sedation of the patient which may result in the loss of protective airway reflexes or ability to
independently maintain adequate ventilatory function. These effects are often unpredictable and can
be specific to the individual, regardless of the dose administered. Staff should be prepared to
appropriately monitor for and manage sedation levels deeper than what was intended. For this reason
the following monitoring requirements, in addition to regular assessment of the basic vital signs (HR,
RR, BP, and LOC), should be followed as a minimum standard:
1. Equipment to provide resuscitation must be available at all times.
2. ECG, RR, BP, EtCO2 and SpO2 must be continuously monitored any time the patient receives
narcotics, benzodiazepines, or dissociative agents by any route.
3. If conscious sedation is being performed, oxygen is required and continuous EtCO2 monitoring
must be applied.
4. Respiratory rate and quality should be continually monitored in all patients.
5. BP should be measured as per CPG 1.
6. For inhaled analgesics (Penthrox) continuous SpO2 and HR monitoring is recommended. EtCO2
monitoring is not required.
CPG 6.2
MANAGEMENT OF NAUSEA AND

VOMITING
MANAGEMENT AIM
To manage nausea or vomiting with judicious use of anti-emetics where nausea and vomiting may be
detrimental to the patient’s condition. The clinical indicators which suggest the AIM is being achieved
are the following:
1. Prophylactic anti-emetics for long distance aeromedical work, where onset of motion sickness may
be detrimental to a patient’s condition.
2. Early administration of appropriate anti-emetics for acute severe vomiting.
2. Correct any reversible causes
3. Ondansetron is the primary anti-emetic utilized in the prehospital setting.
DRUGS AND INDICATIONS
Type Indication Drug
Phenothiazine Motion sickness Stemetil
Dopamine Antagonist Visceral stimulus: Metoclopramide

GIT Irritations (bacterial and
viral)
Migraine
Serotonin Antagonist Chemo-emetic Trigger Zone Ondansetron

(CNS)
Drug or chemically induced
CPG 6.3 SAFE SEDATION AND MONITORING IN ADULTS
Assessment Considerations Other conditions to consider
 Is the patient hypoglycaemic?  Do I have adequate access to the patient?

 Has basic analgesia been given?  Do I have a multiparameter monitor?
 Negotiation or conflict resolution possible?  Do I have nasal EtCO2 available?
 Am I prepared for emergency tracheal
intubation?
co-morbidities?
Obtain a detailed history
 previous anaesthetics?
 current medications?
 fasting status?
Examine the patient thoroughly;  drug use?
focus on:  drug allergies?
 vital signs
 mental status
 cardio-respiratory assessment Continously re-assess risks to the sedated
 patient:
 potential for unintentional loss of con-
sciousness?
Apply monitoring as soon as possible:  depressed airway reflexes?
 SpO2  unpredictable responses due to drug
 EtCO2 effects/ interactions?
 BP  depressed cardiovascular system?
 4-Lead ECG  inadequate analgesia?
REPEAT VITAL SIGNS EVERY
5 MINUTES
Assess the airway and ensure adequacy of

ventilation and perfusion
Administer sedation according to relevant CPG and patient needs
All sedated patients should be managed in the lateral position or 45 degree head,
up unless intubated!
AP & CCP CCP
CPG 6.3
SAFE SEDATION AND MONITORING

IN ADULTS
MANAGEMENT AIM
To provide safe sedation to all patients prior to/during any painful, distressing and/or life-saving proce-
dures, or any clinical situation necessitating chemical restraint.
1. The adult patient is provided with adequate sedation to relive pain / distress during painful/dis-
tressing procedures or situations.
2. Sedation does not negatively impact on the oxygenation or haemodynamic status of the patient.
3. Continuous nasal or in-line capnography is used wherever patients have received light sedation,
deep sedation, dissociative sedation and general anaesthesia.
4. All patient vital signs are continuously monitored. Minimum monitoring includes 4-lead ECG, NIBP
and pulse oximetry.
ASSESSMENT CONSIDERATIONS AND PRECAUTIONS
The initiation of sedation by the clinician requires CAREFUL ATTENTON to all aspects of risk assess-
ment. During procedural sedation, sedatives or narcotics administered to allow the patient to tolerate
unpleasant procedures can result in respiratory and cardiovascular compromise. The risks associated
with sedation include:
 potential for unintentional loss of consciousness;
 depressed airway reflexes;
 inadequate oxygenation;
 unpredictable responses due to drug effects and/or interactions;
 depressed cardiovascular system
 inadequate analgesia;
 individual variation in responses and dosage requirements.
If inadequate oxygen levels are not recognized immediately, the patient may become hypoxic. The
continuous monitoring of respiratory status provides an early warning of respiratory compromise,
allowing the paramedic the opportunity to employ corrective measures before the onset of respiratory
depression, potentially leading to bradypnoea, apnoea, hypoxia or death.
Furthermore, unanticipated mechanical ventilation can lead to increased length of hospital stay and
risk of hospital-acquired infections.
Indications for the use of sedation in adults:
1. Painful or emotionally disturbing/distressing clinical procedures in conscious adults.
2. Consider when splinting fractures or dressing significant soft tissue injuries
3. Safe management of patients who pose a danger to themselves or others (CPG 11).
4. Emergency Rapid Sequence Intubation (CPG 2.3) and maintenance of an established and patent
ETT.
Sedation is a continuum, and it is not always possible to maintain patients at a pre-determined seda-
tion depth. This continuum extends from normal alert consciousness to complete unresponsiveness.
The depth of sedation and definitions are as follows:
1. Minimal sedation (anxiolysis) is a drug-induced state leading to mild cognitive/coordination impair-
ment with unaffected ventilator and cardiovascular functions.
2. Moderate sedation/analgesia (‘Conscious sedation’) is a drug-induced depression of conscious-
ness (the patient generally responds to verbal commands or tactile simulation). The airway is
self-maintained and cardiovascular function is usually maintained.
3. Deep sedation/analgesia is a drug-induced depression of consciousness where the patient can-
not be aroused easily but may respond purposefully to repeated/painful stimulation. Ventilation is
impaired and the patient may require assistance in maintaining a patent airway. Cardiovascular
function is usually maintained.
4. General anaesthesia is a drug-induced loss of consciousness during which patients are not arous-
able, even by painful stimulation. Patients will require airway protection and positive pressure ven-
tilation due to depression of spontaneous ventilation or drug-induced depression of neuromuscular
function. Cardiovascular function may also be impaired.
5. Dissociative sedation: Ketamine is a unique drug in sedation practice because it causes a disso-
ciative state that does not fit the standard definitions listed above. Dissociative sedation is defined
as a ‘trance-like cataleptic state characterized by profound analgesia and amnesia, with retention
of protective airway reflexes, spontaneous respirations, and cardiopulmonary stability’. As there
is loss of verbal contact with patients during Ketamine sedation and because significant (although
rare) complications can occur unpredictably, Ketamine sedation is grouped with deep sedation/
general anaesthesia.
Generally, moderate sedation will be optimal in most situations. Deep sedation is to be avoided as it
is usually unnecessary in the prehospital environment. Most, if not at all, patients in the pre-hospital
setting are not fasted and are therefore at a greater risk of aspiration.
Patients in whom conscious sedation is intended

have the potential to become more deeply sedated.
Be prepared for these situations escalating to the need
for airway protection.
PROCEDURE
1. Obtain a detailed history with particular attention to:

 co-morbidities
 previous anaesthetics
 current medications
 fasting status
 drug use
 drug allergies
2. Thoroughly examine the patient, especially focusing on:
 Vital signs
 Mental status
 Cardio-respiratory assessments
3. Eliminate other factors that precipitate the need for sedation, such as:
 hypoglycaemia
 negotiation or conflict resolution
 basic pain relief measures
4. Prior to, or as soon as practical after sedation, monitor and record the vital signs every 5 minutes
(non-intubated):
 SpO2
 EtCO2 (mandatory in ALL sedated patients)
 BP
 4-lead ECG
 HR/ PR
5. Administer oxygen to ALL sedated patients, who may potentially experience a fall in oxygen sat-
uration from the baseline level measured on room air. Oxygen should be given from the start of
sedative administration until the patient is delivered to hospital.
6. Assess and regularly re-assess the patient’s airway and ventilation status.
7. All patients who are sedated should be managed in the lateral position unless they are intubated,
or an alternative position is required for a procedure.
CPG 7
MANAGEMENT OF HYPERGLYCAEMIA
AND HYPOGLYCAEMIA
MANAGEMENT AIM
To recognise hyper or hypoglycaemia and manage blood sugar levels using appropriate therapy. The
clinical indicators which suggest the AIM is being achieved are the following:
1. Recognising hyperglycaemia or hypoglycaemia.
2. In hyperglycaemia administration of appropriate fluid therapy.
3. In hypoglycemia early administration of appropriate oral or IV carbohydrate therapy.
2. Place the patient in a lateral position if the patient has a decreased level of consciousness.
3. If patient has signs of diabetic ketoacidosis or severe hyperglycaemia (RBS >11mmol/L) consid-
er administering normal saline IV infusion giving 500ml over 10-15 minutes and repeat if the BP
remains low.
4. If the patient has hypoglycaemia (RBS < 4.0mmol/L)
 If cooperative, administer oral dextrose gel.
 If unconscious administer IV 10% dextrose (150-200ml initial dose.) Administer this over 10
minutes, monitoring the RBS as required. Administer additional dextrose if the hypoglycaemia
persists. Avoid causing hyperglycemia.
 If unable to obtain IV access and Glucagon is available, administer 1mg Glucagon IM.

CPG 8
MANAGEMENT OF DRUG OVERDOSE

AND POISONING
MANAGEMENT AIM
To treat the symptoms while trying to identify the toxin/ poison/ drug and if available administer an an-
tidote to limit end organ dysfunction or damage. The clinical indicators which suggest the AIM is being
1. Recognising a poisoning/ overdose has occurred.
2. Initiate symptomatic and specific antidote treatment where available.
3. Transport to an appropriate facility.
Toxicology is an extensive topic covering millions of chemicals, gases, poisons and drugs. The scope
of which is beyond these guidelines. Very few of these have any specific antidote or treatment.
1. Drug overdoses. An overdose occurs when the medication dosage taken exceeds the therapeutic
level and enters the toxic range of the drug. This may be accidental or purposeful.
2. Poisons are substances that have a damaging effect on the body – even in small quantities.
3. A chemical is toxic when it produces a damaging effect (either structurally or functionally) on one
or more body systems.
Assessment of the patient involves monitoring the patient for abnormal signs and symptoms. Attempt
to get a clear history if possible and trying to identify the toxin, poison or drug but do not delay treat-
ment, as it may be difficult to identify the exact substance and most poisonings and overdoses will
require symptomatic treatment

2. For Organophosphates and Carbamates:
 The patient may present with the following clinical appearance:
» SLUDGE (Salivation, lacrimation, urination, defecation, GI pain and emesis)
» Killer “B”s (Bradycardia, Bronchorrhoea, Bronchoconstriction)
 Management:
» Safety – wear protective clothing and gloves. Remove contaminated clothing and rinse any
residual OP compounds off the patient.
» Protect the airway and suction as required. Use a non-depolarizing NMB agent (Rocuroni-
um) if RSI (CPG 2.3) is required.
» Manage bronchoconstriction (CPG 3.1).
» Administer Atropine every 5 minutes until bradycardia and/or excessive secretions are
resolved. Large doses may be required. (Aim for SBP of 90mmHG, HR of 100-120,
and pupils midsize).
 Opioids:
» The patient may present with the following clinical appearance in overdose:
 Classic triad of coma, miosis (pinpoint pupils), and respiratory depression
 Hypotension
» Management:
 Open the airway and assist ventilation with a BVM and oxygen if apnoeic.
 Administer Naloxone 100mcg boluses IV to reverse respiratory depression without
precipitating acute withdrawal symptoms. If IV access unavailable, administer IM/IN
Naloxone.
 Beta Blockers/ Calcium channel blockers
» The patient may present with the following clinical appearance in overdose:
 Bradycardia and hypotension (or both)
 Heart blocks (Ca channel blockers more commonly)
 CNS effects – depression, psychosis and seizures (Severe Beta Blocker OD)
» Management:
 Ascertain history especially of dosage and timing of drug ingestion.
 Establish a large bore IV line and give a fluid bolus (250-500ml NS) if hypotensive.
 Administer Atropine for bradycardia.

 Calcium Chloride IV slowly in 10 min.
 Administer Noradrenaline or Adrenaline/ Epinephrine infusion.
 Carbon Monoxide
» The patient may present with the following clinical appearance:
 CNS – headache, lethargy, emotional instability, nausea, loss of concentration, dizzi-
ness, coma, seizures.
 CVS – chest pain from ischaemia, arrhythmias and palpitations, hypotension and cardi-
ac arrest.
 Use rainbow sensor on the monitor to check carboxyhaemaglobin levels (SpCO)
 Management:
» Establish diagnosis.
» If in cardiac arrest begin CPR.
» Provide 100% oxygen via non-rebreather mask regardless of SpO2 as CO₂ in the blood
will give a falsely high reading.
» If unconscious RSI (CPG 2.3) and ventilate with 100% oxygen.

CPG 9
CLINICAL APPROACH TO THE ADULT

TRAUMA PATIENT
The Clinical Approach to the adult trauma patient lays the foundation for identifying life-threatening
injuries and prioritizing transportation needs. This ensures that only those prehospital interventions
critical to patient survival and/or those that prevent further deterioration during transportation are per-
formed rapidly, with minimal delay of transport.
RESPONDER SAFETY
 Standard and Environmental Precautions (see SOP 2.1)
 Observe for any dangers (dangers to crew, patient and bystanders)
 Observe number of patients and need for additional support (additional resources, police, civil
defence)
PRIMARY SURVEY
Triage the trauma patient in the following manner:
 General impression of the scene (one or many victims, significant mechanism of injury)
 If risk of cervical spinal injuries present (based on mechanism of injury) provide cervical spinal
motion restriction by asking your partner to stabilize the head
 Observe for presence of any Catastrophic Haemorrhage requiring immediate bleeding control
(CPG 9.2)
 Assess level of consciousness as per CPG 1.1

 Assess Breathing status:
» Observe general impression of breathing pattern, rate and signs of distress
If unresponsive, no breathing, no pulse and no confirmation of irreversible death consider starting
CPR (CPG 9.1)
 Assess circulation looking for signs of shock (CPG 9.2)
 Rapid assessment of the mechanism of injury, observed or obtained from the patient or by-
standers.
 Rapid trauma survey assessing for potential internal bleeding (neurological, chest, abdominal,
pelvic and long bone injuries): This assessment should be undertaken in less than 30 seconds.
This assessment focuses on the parts of the body where significant life threatening injuries can
occur:
» Head: Assess level of consciousness (AVPU), pupil symmetry and bleeding associated
with facial fractures which may compromise the airway.
» Neck: Obvious significant bleeding and tracheal alignment. Jugular distension in the supine
patient is normal thus not a significant finding.
» Chest: Palpate the ribs for mobility and tenderness suggesting fractures and check for
open sucking wounds. Assess the work of breathing, symmetry and air entry in 3 places
bilaterally – anterior chest just below clavicles (upper lobes), mid-axillary line in the axilla
(middle lobes) and posterior side next to spine mid-thorax (lower lobes). Percussion in the
prehospital environment is of little value due to ambient noise.
» Abdomen: Palpate for tenderness and rigidity and observe for distension. Look for pene-
trating wounds or evisceration.
» Pelvis: If patient alert, ask about pelvic pain and carefully palpate in the lateral position by
gently pushing on the iliac crests – any pain or movement should be assumed to be due to
fractures.
» Femurs: Gentle pressure applied across the femurs bilaterally looking for tenderness /
movement suggestive of fractures. Observe for swelling of the thigh muscles suggestive of
internal bleeding.
INITIAL MANAGEMENT

 Manage any significant external haemorrhage with direct pressure, wound packing dressing or
tourniquet (CPG 9.2)
 In patients responding to Pain or Unresponsive, open the airway using a jaw thrust, suction the
airway if blood or vomitus present, and maintain airway (options include: OPA or LT in cardiac
arrest)
 Obtain basic vital signs (BP, HR, RR, SpO2) after addressing immediate life threats found
during the primary survey

 Provide Oxygen as per CPG 3.3 if indicated (considering hypoxia or respiratory distress)
 Assess for pain and consider analgesia to reduce patient anxiety (CPG 6.1)
Provide NCC with a situation report including the following:
 Exact location and nature of incident (note any dangers encountered)
 Patient age, gender (also include patient status i.e. VVIP etc)
 Provisional Diagnosis or Chief Complaint (Head injury, trauma arrest etc)
 Trauma triage (red, yellow, green – as per the Primary triage tool)
 If any CCP / Delta / other services (Police, Civil Defense) support is required
SECONDARY SURVEY
 General history: The general history may be initiated during the primary survey and completed
in the secondary survey. It includes history of medications used (prescription, over the counter
and alternative medicines), Allergies, and other relevant past medical or surgical history.
 Level of consciousness: Calculate the GCS of the patient. Repeat if the patient shows signs of
deterioration or improvement.

GLASGOW COMA SCORE ASSESSMENT
Eye Opening
Spontaneous 4
To voice 3
To pain 2
None 1
Verbal Response
Orientated 5
Confused 4
Inappropriate words 3
Incomprehensible sounds 2
None 1
Motor Response
Obeys commands 6
Localizes to pain 5
Withdraws from pain 4
Flexion to pain 3
Extension to pain 2
None 1
/15
Total Score
 Head to toe survey: The head to toe survey is undertaken for completeness especially in the
trauma patient where minor injuries may be overlooked. As the procedure name suggests it
is a systematic assessment of the patient starting at their head down the body to the legs and
then concluded by assessing their back while packaging for transport. The process is used to
assess for deformities, open wounds, tenderness and swelling. Avoid unnecessary log-rolling
especially in high-index suspected blunt spine trauma or suspected pelvic fracture.
ONGOING MANAGEMENT
 Consider establishing IV line for drug access or fluid therapy if required.
 Avoid administering large volumes of Normal Saline unless the patient is in cardiac arrest.
Large volume NS administration is associated with worse outcomes in trauma patients. Con-
sider hypotensive resuscitation targets (SBP 80-90mmHg). Boluses should be in 250ml to
500ml increments.
 If patient meets trauma bypass criteria, bilateral IV placement at the antecubital fossa with
large bore cannula (18g or larger) is recommended. If the patient has poor vascular access on
inspection, a smaller gauge IV may be utilized. In time critical patients (actual or emergent) do
not delay transport to initiate IV access, perform cannulation en route if possible.
 Provide specific management (as per Clinical Guidelines)
 Ensure scene time is appropriate for patient condition (see below)
 Transport to appropriate facility with pre-notification if required (as per trauma bypass criteria
below)
 Consider time to hospital vs time to rendezvous with CCP (do not unnecessarily delay trans-
port)
 If patient refuses transport or further care follow SOP 4.8D for on-scene discharge
ONGOING ASSESSMENT AND MONITORING
1. Complete detailed history (full AMPLE history)

2. Complete relevant clinical examination (repeat secondary survey)
3. Ongoing communication with the patient and family
4. Regularly reassess patient condition, response to treatment and vital signs.
5. For transported patients a minimum of 2 sets of basic vital signs (RR, BP, HR, SpO2, LOC) and
pain score should be obtained unless the patient refuses. Note: performance of basic life-saving
interventions such as chest compressions, hemorrhage control, clearing the airway or moving the
patient into the hospital or out of an immediately dangerous environment etc. should not be de-
layed or interrupted in order to obtain vital signs.
6. Ideally, a set of vital signs will be recorded at least every 15 minutes in stable patients (those meet-
ing the “potential” definition below and not meeting trauma bypass criteria) and every 5 minutes in
unstable patients (those meeting the “actual” or “emergent” definitions below or who meet trauma
bypass criteria). Remember, this is a guideline and the appropriate interval for vital signs obser-
vation is dependent on the patient’s condition and weighed against the need to perform higher
priority interventions.
7. A set of vital signs should be obtained before and after medication administration. Note: Life-sav-
ing medication should never be delayed in order to obtain a full set of vital signs. (Example: if a
blood pressure or SpO2 cannot be obtained due to poor perfusion in the case of life threatening
hemorrhage, fluids should be started)
8. During transport continuous monitoring of SpO2 and ECG (rate and rhythm) in addition to other
basic vital signs monitoring (RR, BP, LOC) is indicated based on the patient’s condition and inter-
ventions performed. A guide cannot be written to anticipate all cases where continuous monitoring
may be indicated. It is recommended to take a cautious approach. As a minimum any patient
who meets trauma bypass criteria, or who has received IV medications with sedative or paralytic
effects (narcotics, benzodiazepines, dissociative agents, paralytic agents) must have continuous
SpO2 and ECG monitoring along with measurement of BP and RR at regular intervals until care is
transferred at the receiving facility.
9. Continous EtCO2 monitoring is mandatory any time an invasive airway is placed or maintaine
(LTA, ETT, Cricothyrotomy), any time narcotics and benzodiazapines are administered to the same
patient in the emergent setting, or anytime a paralytic agent is administered. If time allows, EtCO2
should be monitored if non-invasive ventilatory support is provided (CPAP, BVM). For the CCP,
awake EtCO2 monitoring utilizing a specialized nasal canula is strongly encouraged and must be
immediately available in any patient with moderate to severe respiratory distress or any time medi-
cation is administered which may result in sedation.
10. Identifying a “Time Critical” patient is based on the severity of a patient’s condition or the likelihood
of deterioration. This identification directs appropriate treatment and the appropriate destination to
improve outcome.
TIME CRITICAL DEFINITIONS
Actual: At the time the patient assessment is undertaken, the patient is in actual physiological
distress.
Emergent: At the time the patient assessment is undertaken, the patient is not physiologically
distressed but does have a Pattern of Injury which is known to have a high probability
of deteriorating to actual physiological distress
Potential: At the time the patient assessment is undertaken, the patient is not physiologically
distressed and there is no significant “Pattern of actual Injury”, but does have a Mecha-
nism of Injury known to have the potential to deteriorate to actual physiological distress.
Patients meeting the criteria for Major Trauma should be triaged to the highest level of Trauma care
available. This will in most cases be Hamad General Hospital (HGH) Trauma Resuscitation Unit
(TRU). The receiving hospital must also be notified to ensure an appropriate reception team and facili-
ties are available.
TRAUMA BYPASS CRITERIA
If ONE or MORE of the listed criteria are met, you should immediately notify the CTL and transport
patients DIRECTLY to HGH Trauma Resuscitation Unit, effectively bypassing the HGH RIAMS room/
Bay 1; and/ or bypassing other closer hospitals.
Any deviation from these criteria MUST be authorized through CTL.
If NONE of the listed criteria are met, transport patient to closest hospital emergency department.
ASSESS MECHANISM OF INJURY

Falls:
 Adult fall: 6 meters (20ft or 2 stories), or higher
 Child fall: 3 meters or higher (10ft or 1 story) or twice patient’s height,
 Fall from horse, camel or similar type of animal
Motor Vehicle Crash with:
 Traumatic death in the same vehicle (except bus or mini-bus type of vehicle)
 Significant intrusion > 30cm into the occupant compartment or > 45cm at any site
 Ejection (partial or complete) from vehicle (including ATV-type vehicle)
 Person trapped under vehicle and/ or extrication > 20min
 Rollover with roof deformity > 40cm
Motorcycle accident with speed > 30km/h
Pedestrian/ paediatric/ bicyclist struck by vehicle (thrown/ run over/ or with impact with speed
> 20km/h)
Burns with evidence of trauma OR > 20% BSA in adults OR >10 % BSA in children OR any significant
neck/ facial burns with potential airway compromise.
Hanging or near-hanging with evidence of trauma (eg. hanging fall greater than height of patient or
obvious spine deformity).
Drowning or near-drowning with evidence of trauma (eg. diving into shallow water).
ASSESS VITAL SIGNS AND LEVEL OF CONSCIOUSNESS

1. Glasgow coma scale < 15 (consider effects of alcohol/ drugs)
2. Sustained systolic blood pressure:
 < 90 in adults
 < age-specific normal value in children
 < 110 if age > 65yrs.
3. Respiratory rate:
 < 10 or > 29 in adults
 infant to 1 year old < 20
 any patient needing respiratory assistance
ASSESS ANATOMIC CRITERIA (PATTERN OF INJURY)

1. Chest wall instability or deformity (e.g. flail chest).
2. Traumatic amputation above wrist or ankle.
3. Penetrating trauma to head, neck, torso or extremities above elbow or knee.
4. Open and/ or depressed skull fracture.
5. Suspected pelvic fracture/ unstable pelvis.
6. Neurological deficit in patients with spinal trauma.
7. Two or more fractures of either the humerus or femur.
8. Crushed, de-gloved, mangled or pulseless extremity.
ASSESS SPECIAL PATIENT OR SYSTEM CONSIDERATION

Patients who have sustained significant trauma but do not fit any of the criteria above but are:
 Older patients (> 65 years)
 Pregnant (> 20 weeks)
Is there a reasonable clinical concern despite clearing all of the above criteria AND the CTL is in
agreement?
CPG 9.1
ADULT TRAUMA PERI-ARREST/

CARDIAC ARREST MANAGEMENT
MANAGEMENT AIM
To recognise patients for whom resuscitation is indicated, immediately initiate intervention to restore
perfusion to the brain and other organs and terminate resuscitation when appropriate interventions
have failed to achieve any result or after return of spontaneous circulation. The clinical indicators
which suggest the aim is being achieved are the following:
1. Recognition of a viable patient for resuscitative efforts.
2. Correcting any reversible causes of traumatic peri-arrest/ cardiac arrest, especially hypovolaemia.
3. Recognition of medical cardiac arrest in a situation presenting as trauma.
4. Optimisation of external cardiac compressions, ventilation and electrotherapy in accordance with
the latest international guidelines on resuscitation, ensuring that hypovolaemia has been correct-
ed.
5. Return of spontaneous circulation with a palpable central and peripheral pulses, or termination of
resuscitation efforts when no response to therapy is apparent.
6. Ongoing monitoring and management of reversible causes to prevent re-occurrence of cardiac
arrest.
7. Transportation to an appropriate facility with pre-notification.
The approach to a trauma patient differs significantly from the approach to the ‘medical’ cardiac arrest.
It is important to identify any patient, with reversible traumatic causes and thus potentially survivable
trauma, who may benefit from resuscitation.
It is also important to be aware and consider the possibility of a medical condition resulting in the
patient presenting as ‘trauma’. In this context a serious medical condition can co-exist with serious
traumatic injuries.
Targeted resuscitation attempts concentrating on reversible causes should be initiated immediately if
the patient is peri-arrest or signs of life have been observed in the preceding 10 minutes.
As cardiac arrest is a time critical event, with even small delays resulting in death or permanent
neurological disability, rapid recognition of the need to start correction of reversible causes is crucial.
When assessing any unresponsive trauma patient your first task is to differentiate those in peri-arrest/
cardiac arrest and those who do not have signs of undeniable death (evisceration of major organs,
decapitation),
When to commence CPR?

STEP 1 - Determine if the victim is unconscious.
A person is considered unconscious if they do not answer, move or moan to a “shout and shake”. If a
patient is not awake and not moving, immediately tap or shake them on their shoulders and ask loudly,
“ARE YOU OK?” If the person is conscious they are likely to answer, move, or moan, if not the patient
is considered to be UNCONSCIOUS.
STEP 2 – Expose the patient’s chest.
As soon as a state of unconscious is determined – expose the patient’s chest so you can determine
if there is normal equal rise and fall of the chest. (Care should be taken to maintain patient privacy –
particularly in females).
STEP 3 - Assess for normal breathing and circulation.
Look at their exposed chest for at least 5 seconds but not more than 10 seconds. Normal breathing is
equal rise and fall of the chest. Do not try and determine the rate at this stage. If there is no rise and
fall of the chest, or gasps of air usually associated with a snore or grunting noise – this patient is con-
sidered to have no normal breathing. Simultaneously feel for a carotid pulse to determine if the patient
is in true cardiac arrest.
STEP 4 – Confirm cardiac arrest and begin with compressions whilst treating reversible causes.
If at any time during MANUAL compressions, the victim speaks out, moves, or moans, compressions
should be stopped immediately.
When NOT to commence CPR?

Undeniable Death
If the victim presents with evidence of undeniable death, any attempt at resuscitation is futile. You are
not obligated to initiate CPR in situations when death is undeniable. If in doubt, initiate resuscitation
while seeking consultation and advice from the CTL (Clinical Team Leader).
Criteria for undeniable death include: Decapitation, incineration, decomposition, rigor mortis, depen-
dent lividity and evisceration of major organs, and fetal maceration.
1. Initial approach as per CPG 9: Clinical Approach to the Adult Trauma Patient
2. On recognition of peri-arrest/ cardiac arrest immediately and ideally in parallel perform the follow-
ing:
 Immediately provide the following interventions and at the same time (IF ENOUGH STAFF ARE
AVAILABLE) start high quality chest compressions (The benefit of this intervention in traumatic
arrest is doubtful but may be undertaken to reassure the public and relatives)
» Stop major external bleeding (e.g. tourniquets – perform before starting chest compres-
sions if single rescuer)
» Bilateral chest decompressions (Perform before starting chest compressions if single res-
cuer. Do not perform if isolated head trauma.) (Ambulance Paramedic can only perform
needle decompression under direct CCP supervision)
» Apply pelvic binder.
» Establish IV/IO access and give 2 litres of normal saline as fast as possible.
 Insert LT and oxygenate patient.
 Consider tracheal intubation when practical. Use of muscle paralysis only in the unconscious
patient is acceptable.
The exact order will be determined by circumstances but standard ALS approach is a futile interven-
tion unless potential tension pneumothorax and hypovolaemia have been corrected. In this context
airway management takes second place.
Attach monitoring when practical and assess rhythm. Continue resuscitation as per the adult medical
CPR guideline (CPG 4.1) without the use of the LUCAS II.
Note: If you decide to move the patient to hospital, place the LUCAS II on the patient to provide chest
compressions during transport.
TRAUMA CARDIAC ARREST MANAGEMENT
Note: Continue treatment as per medical cardiac arrest
without the LUCAS device. Use the LUCAS if transporting
with ongoing CPR.
Remember to change person delivering chest compressions

every 2 minutes to ensure high quality chest compressions.
CONDITIONS FOR CONSIDERING TERMINATION OF RESUSCITATION:

Prolonged prehospital CPR that is clearly without any benefit may ONLY be terminated if the following
5 conditions are met. (Note: All 5 must be met.)
1. 20 minutes of continuous asystole despite ACLS CPR.
2. Reversible causes treated.
3. Cardiac arrest not from drug overdose and/or hypothermia.
4. Family or patient’s significant other gives verbal consent (if available).
5. Confirm with CTL if no CCP on scene (in the case of APs).
No breathing and no pulses must be confirmed by

at least 2 HMCAS attendants.
The aim of managing poly-traumatic cardiac arrest is
to treat or reverse potential or possible injuries
and NOT just to treat what you find!
CPG 9.2
MANAGEMENT OF SIGNIFICANT
HAEMORRHAGE AND HAEMORRHAGIC
SHOCK
MANAGEMENT AIM
The aim in the management of significant haemorrhage and haemorrhagic shock are as follows:
1. Recognize significant external and internal haemorrhage with an associated state of shock.
2. Once recognized, the cause of shock needs to be identified and corrected (haemorrhage control)
where possible.
3. Treatment is aimed at haemorrhage control and managing the shock state by providing adequate
oxygenation, ventilation, controlled fluid and vasopressor resuscitation. A patient with uncontrolla-
ble haemorrhage is a time-critical trauma patient requiring swift and safe transport to an appropri-
ate hospital.
The C-ABC (Catastrophic haemorrhage control, Airway, Breathing, Circulation) principle is used to
provide interventions for life-threatening conditions in a priority based systematic manner. The con-
trol of significant haemorrhage must occur as early as possible to increase the chance of survival.
All interventions discussed in this guideline are directed at haemorrhage control and clinical decision
making in the patient with significant haemorrhage.
1. Unexplained signs of shock (SBP< 90mmHg and pulse >110bpm) following a traumatic mecha-
nism of injury without obvious signs of neurological dysfunction (neurogenic shock – CPG 9.7):
 Agitation
 Weakness and light-headedness
 Thirst
 Pale mucous membranes (inside of mouth or eyelids)
 Tachycardia
 Diaphoresis
 Tachypnoea
 Weakened peripheral pulses or dropping blood pressure
2. Injuries associated with significant internal haemorrhage:

 Significant Mechanism of Injury (see CPG 9: trauma bypass criteria)
 Multiple rib fractures/ flail chest
 Open chest injuries
 Blunt or penetrating injuries to the abdomen with guarding, distension or bruising
 Painful pelvis or mobility on assessment
 Bilateral long bone fractures (closed) – especially the femurs.
1. Initial approach as per CPG 9: Clinical Approach to the Adult Trauma Patient:
2. Identify significant external (obvious) or internal haemorrhage. The majority of extremity wounds
will respond to compression, elevation, and/or splinting but when arterial bleeding occurs (e.g.
traumatic amputation), use the combat application tourniquet (CAT). Unstable pelvis must be se-
cured using a pelvic splint (CPG 9.6).
3. Seal any open sucking or blowing chest wounds with a chest seal. Decompress the chest if a ten-
sion pneumothorax is suspected (CCP Only). Post RSI, maintain sedation and paralysis for
mechanical ventilation. This can produce a labile BP, be extra vigilant, especially when managing
traumatic brain injury.
4. Maintain airway. Consider RSI if indicated. Ensure you resuscitate before you intubate. If patient is
haemodynamically unstable (eg: major internal haemorrhage) and maintaining their own airway, and
transport time to the TRU is short, consider rapid transport to the TRU.
5. Assess haemodynamic status for signs of shock (SBP<90 and pulse >110bpm).
 Establish intravenous access using large-bore cannulae, provide isotonic fluid resuscitation,
and assess the patient’s response. Consider intravenous access enroute to hospital. For
major (compressible or non-compressible) haemorrhage administer 250ml fluid boluses to a
maximum of 1L.
 Consider Noradrenaline to achieve MAP ≥65mmHg / SBP 80-90mmHg if unresponsive to
fluids. The presence of radial pulses is a good indicator of adequate perfusion. Do not
attempt to restore normotension.
 In the case of TBI with signs of raised intracranial pressure and major haemorrhage
(polytrauma), administer fluids and Noradrenaline to maintain MAP ≥65 mmHg.
6. Efforts should be made to maintain normothermia in shocked patients. Turn off the air conditioning
to prevent hypothermia.
7. All patients with pain need to be given analgesia (Penthrox / Fentanyl / Ketamine) and this can be
supplemented in transit with further doses of Ketamine, IV or IO. Analgesia is mandatory (except
when a conscious patient explicitly refuses analgesia) before manipulation of fractures.
8. If major hemorrhage suspected, administer anti-fibrinolytic therapy (Tranexamic acid) if the injury
is less than 3 hours old and the patient is aged 14 or over. Dose is 1 gram in 100ml over 5-10
minutes.
9. Tranexamic acid should be given to patients aged 14 or over after sustaining trauma and who
fulfils ANY of the following criteria:
 Systolic blood pressure < 90mmHG or a loss of radial pulse AND/OR
 Pulse rate > 110bpm AND/OR
 Considered to be at high risk of haemorrhage. Patients with high risk or haemorrhage may include (but are not
limited to):
• Open or flail chest
• Crushed, degloved or mangled limb
• Fracture of either one or more of the humerus or femur
• Amputated limb
• Penetrating wound to head, neck, chest, abdomen, or proximal aspects of limbs
• Evidence of catastrophic haemorrhage
• Possible pelvic fracture
• Any significant haemorrhage not controlled by direct pressure or tourniquet
• Any other injury where there is a perceived high risk of haemorrhage based
on CCP clinical judgement.
10. DO NOT administer Tranexamic acid in the following patients:
 Children under 14 years old
 Isolated head injury
 Obvious resolution of haemorrhage
 Allergy to Tranexamic Acid
CPG 9.3
MANAGEMENT OF HEAD TRAUMA AND

TRAUMATIC BRAIN INJURY
MANAGEMENT AIM
Management of Traumatic Brain Injury (TBI) is aimed at preventing secondary neuronal insults and
protecting living brain tissue. This is achieved by:
1. Appropriate airway management and oxygenation (SpO2 ≥ 95%)
2. Ventilation to normocapnia (EtCO2 35-40 mmHg).
3. Correction of hypovolaemia and/or hypotension with isotonic fluids to normotension. Attempt to
maintain Mean Arterial Pressure (MAP) ≥70-80mmHg.
4. Swift and safe transport to an appropriate hospital for further management.
1. Initial approach as per CPG 9: Clinical Approach to the Adult Trauma Patient.
2. Assess the airway: In patients with severe TBI, inability to maintain an adequate airway, or hypox-
aemia not corrected by supplemental oxygen, perform intubation by Rapid Sequence Intubation
(CPG 2.3.)
3. Establish intravenous access en route using large-bore cannulae and provide intravenous fluid
resuscitation as required.
4. Expose patient to assess for other injuries (consider patient dignity). Position the trolley 15º head-
up.
 Maintain MAP 70-80mmHg using Noradrenaline infusion if isolated TBI.
 Maintain MAP of ≥65mmHg using noradrenaline infusion if TBI with major haemorrhage/ haemorrhagic
shock (Refer to CPG 9.2).
5. Specific cerebral herniation management:
 Avoid routine or prophylactic hyperventilation (EtCO2 < 35 mmHg).
 Assess for signs of cerebral herniation:
» dilated and unreactive or unequal pupils
» extensor posturing or no response on motor exam, or
» progressive neurological deterioration evident by a decrease in GCS by more than 2 points
from the patient’s prior best score in patients with an initial GCS < 9
 In patients who are normoventilated, well oxygenated, and normotensive – and still have signs
of cerebral herniation – initiate a short period of hyperventilation (goal EtCO2 30-35 mmHg) and
reassess. Discontinue when clinical signs of cerebral herniation resolve.
6. Transport to Hamad General Hospital Trauma Resuscitation Unit.
CPG 9.4
MANAGEMENT OF CHEST TRAUMA
MANAGEMENT AIM
To prevent or correct hypoxia, identify intrathoracic haemorrhage, which is uncontrollable in the

prehospital setting and may not be self-limiting, requiring swift and safe transport to an appropriate
hospital for further management. This is achieved by:
1. Appropriate airway management and oxygenation (SpO2 ≥95%)
2. Identification of life-threatening chest injuries and urgent intervention if required.
3. Correction of hypovolaemia and/or hypotension with isotonic fluids, to a MAP of ≥ 65mmHg / SBP
80-90mmHg.
4. Swift and safe transport to an appropriate hospital for further management.
2. Assess the breathing: In patients with severe chest injuries and hypoxaemia not corrected by sup-
plemental oxygen, perform RSI (CPG 2.3) and mechanical ventilation (CPG 3.4).
3. Indications for intubation in chest trauma:
 Airway obstruction not corrected by other means.
 Respiratory insufficiency (respiratory rate < 10 or > 30, SpO2 < 95% despite supplemental
oxygen)
 Decreased GCS, especially in associated head trauma: GCS < 8
 Unstable chest wall with paradoxical movement.
 Haemorrhagic shock
 Oral bleeding with decreased protective airway reflexes
4. Assess respiratory rate, effort, air entry and symmetry of chest expansion and administer oxygen
(CPG 3.3).
5. If a tension pneumothorax is identified, decompress the affected side immediately by needle thora-
centesis.
 Anterior 2nd intercostal space, midclavicular line, just above the third rib. Repeat the procedure
1 cm lateral if required. (CCP Only).
 Lateral wall, 4th/5th intercostal space, anterior mid-axillary line. (CCP Only).
6. If an open pneumothorax is identified, close the chest defect immediately with a purpose-made
chest seal.
7. If a flail chest is identified, ensure adequate ventilation.
8. If a haemothorax is identified, assess for signs of shock.
9. Assess haemodynamic status and for signs of haemorrhage and shock and manage accordingly.
10. Establish intravenous access using large-bore cannulae and provide isotonic fluid resuscitation if
required. Consider intravenous access enroute to hospital and permissive hypotension (SBP 80-
90mmHg) in case of uncontrollable intrathoracic haemorrhage.
11. If cardiac tamponade is suspected, consider administration of intravenous fluids to raise venous
pressure and improve cardiac output.
12. Provide analgesia as per CPG 6.1, if no contraindications are present.
CPG 9.5
MANAGEMENT OF ABDOMINAL
EVISCERATIONS
MANAGEMENT AIM
The goal in the management of a bowel evisceration is to:

1. Assess, manage and monitor the patient according to the CABC approach.
2. Realise that uncontrollable intra-abdominal haemorrhage and shock may be present and provide
appropriate interventions and transport.
3. Prevent drying of any protruding organ or viscera.
2. Remove clothing from around the abdominal wound.
3. Cover the wound with sterile dressing soaked with normal saline. Cover the moistened dressing
with a sterile occlusive dressing to prevent evaporative drying.
4. Flex the knees to relax abdominal wall to limit ischaemic injury to eviscerated organ.
CPG 9.6
MANAGEMENT OF PELVIC AND

LONG BONE FRACTURES
MANAGEMENT AIM
The aim in the management of a pelvic and long bone fractures is to:
1. Recognize the presence of these injuries.
2. Protect the patient from disability.
3. Anticipate, prevent or treat any complications such as haemorrhage and shock.
Haemorrhage from long bone and pelvic fractures can be life threatening, thus early identification and
stabilization are an important part of trauma care. Long bone fractures are recognised by:
1. Pain
2. Crepitus
3. Oedema
4. Associated soft tissue trauma
5. Muscle spasms surrounding the fracture
6. MOI suggesting forces capable of producing fractures
For diagnosis of possible pelvic fractures consider the following signs and symptoms:
1. Pain over the pelvic area with:
 Unexplained hypotension without any other identifiable cause
 Progressive flank, scrotal, or perianal swelling and bruising
 Blood at the urethral meatus
2. Instability on movement of the pelvic ring (this should not be tested for if the patient is complaining
of pelvic pain)
3. Failure to respond to initial fluid resuscitation
Pelvic fractures are difficult to diagnose in the field and the risk associated with placing a pelvic binder
on a patient without a fracture is low, therefore a pelvic binder should be placed when the patient has
sustained a high mechanism of injury and has any of the following:
1. Hypotension
2. Pelvic pain
3. Is unresponsive or pain response is unreliable
4. Practitioner suspects presence of fracture
Splinting of pelvic fractures is considered a haemorrhage control procedure and should be done as
soon as a pelvic fracture is suspected, preferably before moving the patient.
2. Assess haemodynamic status especially signs of shock from uncontrolled haemorrhage from the
pelvis or long bones. Use a pelvic binding device to control bleeding from pelvic fractures.
 Establish intravenous access using large-bore cannulae, provide isotonic fluid resuscitation,
and assess the patient’s response. Consider intravenous access enroute to hospital and per-
missive hypotension (SBP 80-90mmHg) in case of uncontrollable haemorrhage.
3. Expose the patient to assess for other injuries. Consider providing analgesia as per CPG 6.1 be-
fore splinting any fractures. Splint long bone fractures with appropriate immobilization equipment.
4. The appropriate device for a femur fracture is the traction splint unless a contraindication to its use
is present.
CPG 9.7 MANAGEMENT OF SUSPECTED SPINAL INJURIES
Assessment Reminders Mechanism to consider
 Are there complaints of:  Any fall from standing or sitting with evi-
dence of striking head
 Neck or back pain?
 Numbness or tingling?  Any fall from height
 Loss of movement or weakness?  Any RTA
 Loss of sensation?  Any trauma where victim was thrown
 Is there:  Any lightning or high voltage injury
 Pain on movement of back or spinal column?  Any diving injury

 Guarding against movement of back?
 Obvious deformity of back or spinal column?
 Weak or flaccid muscles?
 Loss of control of bladder or bowel?
 Erection of the penis (priapism)?
 Neurogenic shock? RESTRICT SPINAL MOTION
 Apply manual in-line head/neck stabili-
zation
YES
 Spinal pain/tenderness or anatomic deformity?
IF AMBULATORY
NO
 Allow patient to slowly move to stretcher
YES mattress with minimal spinal motion.
 Any altered mental status (GCS<15)?
NO IF NON-AMBULATORY
YES  Use scoop stretcher to move patient to
 Signs of intoxication with drugs / alcohol? stretcher mattress with minimal spinal
motion.
NO
 Apply cervical collar and head blocks.
YES
 Patient distracted by other painful injury?
Transport on stretcher mattress WITHOUT
NO LBB if patient ambulatory OR if scoop can
be removed with minimal patient motion.
 Neuro deficit after trauma (S/S of extremity weak- YES
ness/numbness)
NO
 DO NOT RESTRICT SPINAL MOTION
These criteria cannot be assessed on any patient with a language or commu-

nication barrier (including infant/ toddler/ pre-school patients) that prevents
understanding and appropriately responding to the assessment questions. If
in doubt, restrict spinal motion.
CPG 9.7
MANAGEMENT OF SUSPECTED
SPINAL INJURIES
MANAGEMENT AIM
Excessive motion of the spine may worsen spine fractures or spinal cord injuries (especially in pa-
tients with altered consciousness who cannot restrict their own spinal motion), but immobilization on a
long spine board may also cause pain, agitation, respiratory compromise, and pressure ulcers.
Management of Spinal Cord Injury (SCI) is aimed at preventing secondary spinal cord damage. This is
achieved by:
1. Appropriate oxygenation (SpO2 ≥ 95%)
2. Correction of hypovolaemia and/or hypotension with isotonic fluids and vasopressors
3. Careful packaging and immobilization of the patient
4. Safe transport to an appropriate hospital for further management
Based on an index of suspicion from the mechanism of injury undertake a careful assessment of
patient condition looking for signs and symptoms associated with spinal injuries, to determine whether
restriction of spinal motion is required. The following should be considered:
1. Patient Complaints:
 Neck or back pain
 Numbness or tingling
 Loss of movement or weakness
2. Signs Revealed During Assessment:
 Pain on movement of the back or spinal column
 Obvious deformity of back or spinal column
 Guarding against movement of back
 Loss of sensation
 Weak or flaccid muscles
 Loss of control of bladder or bowels
 Erection of the penis (priapism)
 Neurogenic shock
3. If the patient meets all of these criteria below, the risk of spinal injuries being present is very low
and they can be transported without spinal motion restriction:
 The patient must be awake and alert
 The patient must not be intoxicated or under the influence of drugs
 The patient must not have any painful distracting injuries (other bony fractures or significant
soft tissue injuries)
 The patient must not have tenderness over the spine on palpation
 The patient must not have any neurological symptoms (localised paraesthesia, weakness or
paralysis)
4. Exclusion criteria (the following types of patients should NOT be immobilized)

 No history or no mechanism of injury that would be consistent with spinal injury
 Patients with penetrating trauma to the chest, abdomen, head, neck or back. These patients
may be harmed by immobilization.
 Patients with gunshot wounds to the head do not require immobilization.
 Patients with non-traumatic back or neck pain related to movement, position or heavy lifting.
2. In patients with high spinal injuries and diaphragmatic breathing, administer oxygen as per CPG
3.3 and consider supporting their ventilation if hypoventilation is present.
3. If signs of neurogenic shock are present:
 Establish intravenous access using large bore cannulae and provide up to a litre of intravenous
isotonic fluid resuscitation. Beware of pulmonary oedema with aggressive fluid administration.
 If intravenous fluids do not improve blood pressure, consider using vasopressors
(Noradrenaline).
 Consider intravenous access enroute to hospital in case of other trauma with uncontrollable
haemorrhage.
4. Use the criteria above in deciding whether spinal motion restriction is indicated.
 LBB use restricted to extricating patients following RTAs.
 Use the scoop stretcher to move patients with confirmed/ high index of suspicion of spinal inju-
ries onto the stretcher and then remove the scoop.
 Use the Head Blocks and C-Collar to maintain head motion restriction - avoid unnecessary
use of cervical collars. If a collar is necessary (e.g. obvious neck deformity), ensure that it is
correctly sized and fitted.
 Do not transport patients on an LBB.
5. Beware – minimal trauma may lead to spinal fractures in patients with advanced age and ground
level fall and also in patients with history of rheumatoid arthritis, severe osteoarthritis, Down’s Syn-
drome, cancer, or ankylosing spondylitis. If these patients meet the spinal clearance criteria then
restrict spinal motion anyway, even if their mechanism of injury was relatively minor.
CPG 9.8
MANAGEMENT OF BURNS
MANAGEMENT AIM
The goal of early management of the burns patient is to:

1. Establish airway control if required or anticipated to be required in the near clinical course.
2. Stopping the burning process.
3. Managing fluid balance through administration of IV fluids to replace lost plasma through the
burned area.
4. Provide adequate pain relief.
DEPTH OF BURN
Superficial Partial thickness Full thickness

(1st degree) (2nd degree) (3rd degree)
Cause Sunburn, minor flash Hot liquids, flashed, or Chemicals, electricity,

burn flame flame, hot metals
Skin appearance Erythema Red or mottled, swell- Dark and leathery or
ing, blisters waxy white, translucent,
or mottled
Painful Painful Painless
2. Stop the burning process:
 Remove the patient from the heat source.
 Remove smouldering and constricting clothing, shoes, and jewellery unless it adheres to the
skin.
 Cool the patient with room-temperature water or saline for no more than a few minutes while
simultaneously initiating the primary survey. Do not use ice or cold water.
 Cover the patient with clean, dry sheets or Burnshield® type dressings.
3. In the case of inhalation burns, the decision to intubate needs to be weighed up carefully with con-
sideration of anticipated clinical course and transport time to hospital. See CPG 2.3 (RSI).
4. Monitor oxygenation with clinical observations and pulse oximetry, however, beware of incorrect
high readings due to CO exposure. Always assume CO exposure in patients who were burned in
enclosed areas. Measure and monitor SpCO if available (SpCO < 10% is considered normal).
5. Establish intravenous access using large bore cannulae and provide intravenous isotonic fluid
resuscitation if required. Consider two IV sites. If establishment of intravenous access is unsuc-
cessful, establish intraosseous access if not contraindicated.
6. Provide up to 1000ml NS over the first hour following injury, in the adult patient.
7. Consider exposing the patient to assess for other injuries if not done so already. Prevent hypother-
mia. Perform a secondary survey.
8. Provide analgesia (CPG 6.1) as per guidelines.
SPECIAL CONSIDERATION: ELECTRICAL BURNS

Electrical burns occur when electricity enters the human body and are frequently more serious than
they appear on the surface of the body.
If the electrical current flows through the heart, life-threatening arrhythmias may ensue. Therefore, ev-
ery patient that received an electric current injury should have an ECG done to assess cardiac activity
and should have continuous 4-lead ECG monitoring during treatment and transport.
CPG 10.1
MANAGEMENT OF HEAT-RELATED
INJURY AND HEAT STROKE
MANAGEMENT AIM
The management aim is to recognise a heat-related disorder and initiate intervention to normalize the
temperature and physiological parameters to prevent end organ damage. The clinical indicators which
suggest the aim is being achieved are the following:
1. Recognising a heat-related disorder, especially life-threatening heat stroke.
2. Initiate cooling, fluid resuscitation and life support interventions.
Heat emergencies are associated with the following clinical findings:

1. Heat exhaustion: dizziness, syncope, tachycardia, hot flushed sweaty skin, nausea and vomiting.
The patient normally remains awake. The core body temperature is below 40ºC.
2. Heat stroke: The patient presents with a decreasing level of consciousness with possible seizures,
core body temperature over 40ºC and hot dry skin if sweating processes have failed.
2. Consider securing the airway if the level of consciousness is depressed. Vomiting is common in
heat stroke and may lead to aspiration. Do not delay cooling and seizure management to secure
the airway, unless there is active vomiting.
3. If seizures are present treat according to seizure guideline (CPG 5.2).
4. Use active cooling processes after removing most of the clothing (remembering where possible to
maintain the required modesty when treating a person of the opposite sex). Place cooling packs
between the thighs, under the axilla and chest and neck as well as sponging the patient with cool
(not cold) water and blow air over them using the vehicle air-conditioner or a fan. Rapidly cool the
patient to about 39ºC then monitor temperature to avoid hypothermia or a further rise in tempera-
ture.
5. Initiate fluid resuscitation with cold fluids if possible. Administer enough fluids (in 250ml NS bo-
luses) to raise the blood pressure to normal levels and restore organ perfusion (this is difficult to
monitor in the pre-hospital environment). Pulmonary Oedema is a risk of excessive fluid resuscita-
tion so careful monitoring is required during fluid resuscitation.
CPG 10.2
MANAGEMENT OF COLD-RELATED
INJURY
MANAGEMENT AIM
The management aim is to recognise hypothermia and initiate intervention to normalize the tempera-
ture and physiological parameters to prevent end organ damage. The clinical indicators which suggest
the aim is being achieved are the following:
1. Recognising a cold-related disorder.
2. Initiate heating, fluid resuscitation and life support interventions.
Cold emergencies are associated with the following clinical findings:

1. Mild hypothermia (CBT >32-35ºC): shivering, excitation, loss of fine motor control, mild confusion
or slow thought.
2. Moderate hypothermia (CBT 28-32ºC): delirium, slow reflexes, confusion, bradycardia, shivering
stops below 31ºC
3. Severe hypothermia (CBT < 28ºC): muscular rigidity, absent reflexes, extremely weak or absent
pulses and breathing, coma, fixed dilated pupils.
2. Careful handling is required as the irritable heart muscle may fibrillate with any rough handling
(bumping).
3. Consider securing the airway if the level of consciousness is depressed. Muscle rigidity may make
intubation difficult and muscle relaxants do not work efficiently below 30ºC CBT.
4. Initiate oxygen therapy (CPG 3.3)
5. Establish a large bore IV line for drug and fluid access – administer 1Liter NS as hypothermic
patients are often fluid depleted.
6. Pack warmed fluid vacolitres into armpits, neck and groin area to provide external warming. Alter-
natively take outside into the heat if it is summer in Qatar. Cover with blankets to maintain heat.
Avoid precipitating hyperthermia.
CPG 10.3
MANAGEMENT OF ENVENOMATION
MANAGEMENT AIM
The management aim is to treat symptomatically. The clinical indicators which suggest the aim is
being achieved are the following:
1. Rapid attempt to identify species (snake, scorpion, marine) of envenomation.
2. Initiate symptomatic airway, respiratory and cardiovascular care.
There are a few species of venomous snakes in Qatar:

1. One species (Horned viper) has both cytotoxic and neurotoxic venom which causes immediate
pain, swelling and bruising. Dizziness and tingling may onset later.
2. The Saw Scaled Viper has haemotoxic venom causing the failure of the clotting system with bleed-
ing from mucous membranes and a risk of intracranial haemorrhage. These symptoms may take a
few days to onset following the bite.
3. Scorpions have neurotoxic venom. Envenomation produces overstimulation of the CNS, sympa-
thetic and parasympathetic nervous systems. The resulting symptoms include local pain, paraes-
thesia, agitation, tachycardia, vomiting, abdominal pain, salivation, diaphoresis, dehydration, mus-
cle rigidity and twitching, tremor, seizures, coma, pupillary changes, hyperthermia, tachyarrythmias
and occasionally bradyarrhythmias, hypertension, and less often hypotension, cardiac failure, and
priapism in males.
4. Neurotoxic spider venom symptoms start within 20 minutes with acute pain at the bite site, se-
vere muscles cramps and abdominal pain may follow, with weakness and tremors. Large muscle
groups are often affected, resulting in considerable pain. In bad cases, victim might even experi-
ence nausea, vomiting, dizziness, fainting, chest pain, and respiratory difficulties.
5. Jelly fish: stings from the tentacles can produce skin irritations and on rare occasions severe aller-
gic reactions.
6. Stone Fish: produces severe pain and in rare cases may be fatal.
2. Assess the patient and the bite site. Monitor for signs of neurotoxic envenomation (respiratory or
cardiovascular failure).
3. Limit the patient’s movement to prevent the spread of the venom.
4. Apply a pressure dressing to the limb from distal to proximal – watch for excessive swelling and
compartment syndrome from tight dressings.
5. Consider establishing an IV (keep vein open) and for fluid management should the haemodynamic
status deteriorate.
6. Administer analgesia as required (CPG 6.1) and Midazolam for muscle spasms from spider bites.
7. Stone Fish envenomation: most commonly affected limb is the foot due to standing on the fish. Immerse
the affected limb in warm water and increase the temperature to the highest temperature the patient can
tolerate or until symptoms are relieved. Administer analgesia as required.
CPG 10.4
MANAGEMENT OF SUBMERSION
INJURY
MANAGEMENT AIM
The management aim is to identify complications associated with a near drowning and initiate inter-
ventions to limit end organ dysfunction. The clinical indicators which suggest the aim is being achieved
are the following:
1. Identify complications associated with a near drowning.
2. Initiate cardio-respiratory resuscitation and other life support interventions.
Some definitions regarding submersion incidents:

1. Drowning: when a person is pronounced dead following submersion or within 24 hours of the inci-
dent.
2. Near-drowning: the person is revived and survives for more than 24 hours following submersion.
Secondary drowning: severe pulmonary oedema

which onsets within 24 hours following
a primary submersion incident.
1. Initial approach as per CPG 1: Clinical Approach to the Adult Medical Patient or CPG 9: Clinical
Approach to the Adult Trauma Patient depending on the history
2. Initial assessment: undertake a rapid assessment of the history (specifically of possible trauma
mechanism, consider c-spine injury in dive related drowning, duration in the water and
temperature of the water).
3. Assess for circulation – if none present initiate CPR as per CPG 4.1 (if no trauma suspected) or
CPG 9.1 (If trauma suspected).
4. Consider securing the airway if the level of consciousness is depressed. Foam from the mouth
is common and presents pulmonary oedema. Suction is not required and clearing the airway will
only exacerbate hypoxia. Provide basic and advanced airway support. Consider CPAP for awake
patient. Vomiting is common following near drowning and may lead to aspiration. RSI if required
according to CPG 2.3 (consider spinal care if trauma mechanism is present).
5. Provide temperature control if hypo/ hyperthermia is present.
CPG 11 MANAGEMENT OF THE COMBATIVE PATIENT
 Is there any condition or injury causing  Hypoxia

behaviour?  Hypoglycaemia
 Emotional/ psychiatric history?  Head injuries/ neoplasms/ infections
 Patient refusing care (patient rights)  Drug/ alcohol use
 Is there a risk to self and/or others?
 Request supervisor and police support

 Attempt de-escalation (calm environment and open communication)
 If de-escalation fails and there is a risk to your safety leave the scene and
notify supervisor.
 Provide oxygen as soon as possible if chemical sedation is considered.
 Ketamine (Preferred drug):

 IM: 5mg/kg (maximum dose 400mg) IM, OR
 IV: 0.25 - 0.5mg/kg boluses (maximum single dose 50mg) which may be
repeated until sedation achieved.
OR
 Midazolam:
 IM: 0.1mg/ kg – up to maximum dose of 10mg per injection, may be
repeated after 15 minutes if required.
 Oral: for the mildly agitated patient, 5-10mg of the IV solution may be
given orally (preferably administered with a fruit juice)
 Continous EtCO2 monitoring is mandatory if chemical sedation is adminis-

tered
 Sedation is not a means to force a person to go to hospital against their will.
 Sedation should not be provided at the family request, unless an obvious
danger to self or others exists.
 Police should assist with physical restraint – as they are trained.
 Do not use physical restraints, unless no other option exists and the patient
and staff safety is compromised, then only sufficient restraint to prevent
injury.
 Never secure a patient on prone, as this may lead to suffocation.
AP & CCP CCP
CPG 11
MANAGEMENT OF COMBATIVE PATIENT
MANAGEMENT AIM
To assess the need for patient restraint and utilise the most appropriate method within the legal and
patient rights framework while maintaining the safety of staff and patient. The clinical indicators which
1. Exclude other causes of combative behaviour.
2. Initiate a management process starting with de-escalation and proceeding on to mechanical or
chemical restraint where required.
3. Mitigate risk of injury to medical staff and the patient during the process.
Aggressive or combative behaviour may be caused by disease, injury or by severe emotional or psy-
chiatric pathology. Practitioners need to manage these patients without overstepping legal boundaries
and exposing themselves to a possible charge of assault brought by the patient or their family.
Restraint is any method used to de-escalate the situation or restrict the movement or activity of the pa-
tient to prevent harm to themselves or others. Techniques used include verbal de-escalation, physical
restraint using limb holders or body straps and chemical restraint. The use of restraint should escalate
from verbal through to chemical unless the patient is an immediate threat to others or self then the
method used should be the one limiting the risk to all.
The level of force used to restrain the patient should be reasonable and justifiable. If physical restraint
devices are used they should be loose enough to prevent injury or neurovascular compromise. Where
prolonged restrain is likely chemical restraint may be used as the primary option with loose physical
restraints as backup. Prolonged struggling against restraints can precipitate severe acidosis and pos-
sible cardiac arrest.
CLINICAL INDICATIONS ACCORDING TO HMC POLICY:
1. Medical/ Trauma:
 Extreme agitation due to physiological cause (hypoxia, hypoglycaemia, head injury), which
cannot be rapidly reversed.
 Lack of insight or understanding (paediatrics, elderly with dementia, etc.)
 Interference with or constant removal of important medical equipment
 Movement which places patient at risk of falling.
2. Behavioral (sedation should only be considered in the circumstances below):
 Agitation, hostility or aggression which places:
• Risk to medical staff
• Risk to themselves
• Risk to others.
1. Assess the situation and call for supervisor, CCP and police backup if a clear safety risk is present.
Do not enter a room if there is a risk of violent behaviour until sufficient staff are available to under-
take physical restraint if required.
2. In medical/ trauma related combativeness exclude all reversible causes before undertaking any
restraint process.
3. Attempt de-escalation techniques:
 Create a safe environment – do not get between the person and their escape route or get
trapped in a corner.
 Communicate with the patient, listening to his complaints and reasons for being angry.
 Offer realistic options to de-escalate the situation – their anger may be due to family trying to
force them to do something against their will.
 Offer voluntary mild sedation/anxiolysis
• IM/IV/Oral Midazolam (see formulary)
 If a weapon is present get the person to place it in a safe place rather than handing it over.
4. If de-escalation is unsuccessful then physical or chemical restraint may be required.
 Physical restraint requires a minimum of 5 people – one for each limb and one person to
support the head and neck to avoid injury. The patient should never be restrained in a prone
position except to gain control and then they should be turned over.
 Arms and legs should be secured separately to the stretcher and the patient should never have
their arms and legs secured together behind their back. Movement can be restricted by placing
straps over the chest and thighs above the knees. The chest straps should not restrict breath-
ing.
 Chemical restraint should be given IM to limit the risk involved with IV insertion. The dosage
given should be enough to create calmness without heavy sedation.
 Careful monitoring is required once a sedation agent has been given to avoid cardiovascular or
respiratory compromise.
1. Vital signs monitoring as per CPG 1.

2. Continuous monitoring of SpO2 and ECG is required if sedation is administered regardless of route
or dose.
3. Continous EtCO2 monitoring is encouraged in all cases where sedation is administered.
4. Monitoring should be applied as soon as patient is calm enough to do so safely.
CPG 12
CLINICAL APPROACH TO THE

OBSTETRIC PATIENT
Your initial approach to the Obstetric patient should be according to:

1. For non-trauma cases: Initial approach as per CPG 1: Clinical Approach to the Adult Medical Pa-
tient or
2. For trauma-related cases: Initial approach as per CPG 9: Clinical Approach to the Adult Trauma
Patient
PHYSIOLOGICAL CHANGES DURING PREGNANCY:

During pregnancy various changes occur to allow the mother’s body to adapt to and assist growth of
the fetus. These changes need to be recognized during physical examination and taken into consider-
ation during the management of pregnant patient.
HAEMATOLOGY:
There is an overall increase in blood volume (approximately 1500ml). During the first trimester, the
blood plasma increases by 15% and peaks at 50% above the normal (32 weeks).
CARDIOVASCULAR SYSTEM:
The heart enlarges due to an increase in blood volume and increase in cardiac output. The heart rate
increase up to 25% by the end of the second trimester. Pressure on the diaphragm displaces the heart
upwards, rotating it forwards and displaced laterally. Due to the placenta acting as arteriovenous shunt
and peripheral vasodilation, systolic blood pressure may drop slightly (6-8%) with a more marked drop
in diastolic blood pressure during the first two trimesters.
The following ECG changes occur during pregnancy (no clinical significance):
 Sinus tachycardia with arterial and ventricular ectopics
 ST segment depression and t-wave inversion in the inferior and lateral leads
RESPIRATORY SYSTEM:
The upper respiratory tract becomes more vascular with oedema and hyperemia developing in the
nose, pharynx, larynx, trachea and bronchi. Maternal oxygen requirements increase. The thoracic
cage, increases by 5 – 7 cm in diameter. The diaphragm is displaced upwards by the enlarging uterus.
Due to the diaphragms inability to descend during inspiration, thoracic breathing replaces abdominal
breathing in late pregnancy. As oxygen consumption increases minute ventilation increase by 40%
with increased respiratory rate and tidal volume from the first trimester to term by a total 45%. Func-
tional residual capacity decreases by 20-30%.
Anatomical and physiological changes in both the cardiovascular and respiratory system causes a
general feeling of breathlessness particular on slight exertion but also consider underlying pulmonary
effects of cardiovascular disease.
UTERUS:
The uterus changes from an initial weight of roughly 70g (10ml) to a term weight of 1.1kg (5L). The
perfusion of the placenta is dependent on maternal circulation to the uterus and as the uterus increase
in size blood flow increases rapidly. The total increase in blood flow to the uterus is up to twenty times
normal. By the end of pregnancy, about a sixth of the maternal blood volume is within the uterine
circulation.
There are various other changes in the renal, gastro-intestinal, integumentary, endocrine and muscu-
loskeletal systems during pregnancy.
OPTIMIZING CARE:
Airway management: The changes to the upper airway, functional residual capacity, airway edema
and a higher likelihood of bleeding will make mask ventilation and endotracheal intubation more
challenging. There is an increased risk of aspiration and the decrease in functional residual capacity
and higher oxygen consumption during pregnancy will result in rapid desaturation during induction for
intubation.
Due to the increase in maternal circulating blood volume, the pregnant patient can lose between 1200-
1500ml of blood or 35% of the blood volume before signs of hypovolemic shock develops and should
be considered in the management of any pregnancy patient with blood loss.
Supine Hypotensive Syndrome occurs with compression of the inferior vena cava and abdominal aor-
ta by the gravid uterus of the pregnancy woman in a supine position, resulting in hypotension, sweat-
ing, pallor, bradycardia dizziness and possibly a loss of consciousness.
Always remember that the unborn fetus is dependent on the mother for oxygenation and perfusion. In
light of the fact that the various physiological changes of pregnancy may delay or mask any signs and
symptoms indicative of maternal deterioration, action to prevent maternal collapse and promote fetal
survival must be taken early. It is important to prevent fetal hypoxia and hypoperfusion of the uterus.
In addition to the above all females of a reproductive age, who presents with vaginal bleeding, should
be considered to be pregnant until proven otherwise.
NOTE: Consider the Cultural and Religious perspectives of the patient and their family, and if required
arrange a female member of staff to undertake the assessment and history taking.
HISTORY TAKING IN OBSTETRIC PATIENTS:
1. Past Medical history:

 Any underlying medical conditions, like hypertension, diabetes, epilepsy, asthma etc.
 Any previous surgeries?
 Any current medication?
 Any family history of complications during pregnancy and/or delivery
 Smoking?
2. Past Obstetric History:
 Details of all previous pregnancy, if any (including miscarriages and/or terminations)?
 Number of previous pregnancies?
 Length of gestation
 Onset of labor (spontaneous or induced)
 Mode of delivery – vaginal or caesarean
 Complications with previous pregnancies (breech presentation, PPH, still birth, neonatal resus-
citation)?
 Length of previous labor
3. Current pregnancies
 Due date?
 Have the membranes ruptured? If yes;
 What time did they rupture?
 What was the colour of the liquor?
 What time did contractions begin?
 W000hat is the frequency and duration of the contractions
 Does the mother have the urge to push?
 Have any complications been identified with this pregnancy? (EG: breech presentation on last
scan, placenta previa (if so, what grade?), multiple fetuses.
 When was the last scan? What position was the fetus in on this scan? (cephalic, transverse or
breech)
 Can the mother still feel fetal movement? If no, how long ago did fetal movement cease?
 Has the mother had antenatal care?
4. Current issues
 PV loss – blood or mucus – volume of blood loss.
 Vital signs – are they within normal limits? Is the mother physiologically stable?
 What is the pain score?
 Did trauma precipitate the commencement of labour?
 Other complaints?
» Nausea/ vomiting
» Full bladder
PHYSICAL ASSESSMENT:
Conduct a general assessment as per CPG 1 / CPG 9 including additional considerations for the ob-
stetric patient:
NORMAL VITAL SIGNS RANGE:
Vital signs Normal range
Blood Pressure Less than 135/85
Pulse Between 60-90 beats per minute, pulse rate increase around 10 beats per
minute during pregnancy
Respiratory Rate 16-24 breaths per min, there may be a degree of hyperventilation
Temperature 36.2º-37.6ºC
The maternal position as well as the size of the blood pressure cuff and maternal anxiety during blood
pressure measuring will affect the reading. Maternal anxiety will result in an elevated blood pressure.
If elevated, the patient should be given time to rest before the BP reading is repeated.
Blood pressure will be highest when the patient is seated and lowest when the patient is in a supine
position. This position may result in the development of supine hypotension syndrome. It is best to
assess the blood pressure of a pregnant patient on the same arm and in the same position during the
prehospital management. The blood pressure should be assessed either with the patient in a seated
position or with the patient in the left lateral position.
MATERNAL EARLY WARNING CRITERIA
Systolic Blood Pressure <90 mmHg >160 mmHg
Diastolic Blood Pressure >100 mmHg
Heart Rate: beats per min <50 >120
Respiratory Rate: breath per min <10 >30
Oxygen Saturation, at room air <95 %
Maternal aggression, confusion or unresponsiveness
An obstetric patient meeting any of the above criteria should be transported promptly and the receiv-
ing facility notified.
ABDOMINAL EXAMINATION:
1. Inspection:
 Inspect for abnormal masses, scars from previous surgery and asymmetry.
2. Palpation:
 Assess the height of the fundus and presence of any abdominal tenderness
 Assess the height of the fundus - the measurement commonly used to estimate gestation is the
height of the fundus, however variations in the position
of the fetus, height of the fundus, amount of amniotic
fluid, presence of more than one baby, maternal obe-
sity and examiner experience reduces its accuracy. It
involves measuring or estimating the distances from the
symphysis pubis to the top of the fundus in cm after 12
– 14 weeks of gestation, which roughly correlates to the
gestational age in weeks.
Figure 1: Fundus height
 Appropriate fundus height landmarks:
» Height of the symphysis pubis – 12 weeks gestation
» Height of the umbilicus – 20 weeks gestation
» Height of the xiphoid process – 36 weeks gestation
» Between 37 – 40 weeks the fundus regress to between 36 and 32cm
INITIAL MANAGEMENT
1. In addition to the management in CPG 1: Clinical Approach to the Adult Medical Patient or CPG 9:
Clinical Approach to the Adult Trauma Patient consider:
 Calm and reassure your patient and her family, it is likely she will be anxious with regards to her
condition. Consider that ANY female of reproductive age with PV bleeding or unexplained lower
abdominal or pelvic pain may be pregnant.
 Allow the patient to assume a position of comfort, ensuring it doesn’t compromise their cardio-
vascular stability. Consider transporting pregnant patients on their Left Lateral position to avoid
Supine Hypotensive Syndrome.
2. Patient destination should be determined by following the Obs/Gynae Bypass Criteria.
OBS / GYNAE BYPASS CRITERIA
OBSTETRICS & GYNAECOLOGICAL RELATED CONDITIONS / EMERGENCIES
1. Active labour at < 31 weeks gestation
WOMENS’ WELLNESS &

RESEARCH CENTER ED
2. Abnormal delivery presentation
3. Prolapsed cord
4. Threatened abortion / ectopic pregnancy
5. Major vaginal haemorrhaging
6. Severe PET (Pre-eclamptic toxaemia) / Eclampsia < 31 weeks
7. Active labour (if patient is currently seen at WWRC OPD or it is
the closest facility)
NOTIFY CTL FOR ALL CASES (1-6) TRANSPORTED TO WWRC

EXCEPT ROUTINE ACTIVE LABOUR (7)
WOMEN’S
NEAREST
ED
Active labour > 31 weeks gestation with NO complications
UNSTABLE patients are to be transported to the nearest Women’s ED for stabilization.

Patients will then be transferred to WWRC via the appropriate route once in a stable condition.
MEDICAL CONDITIONS / EMERGENCIES IN THE PREGNANT PATIENT
APPROPRIATE
CLOSEST
All medical conditions or emergencies NOT related to

ED
obs/gynae complication
TRAUMA EMERGENCIES IN THE PREGNANT PATIENT

HGH TRAUMA
Bypass Criteria)
(As per Trauma
ROOM
All pregnant patients that have sustained trauma

CPG 12.1
MANAGEMENT OF ANTEPARTUM
COMPLICATIONS
CPG 12.1.1
MANAGEMENT OF ECTOPIC
PREGNANCY
MANAGEMENT AIM
To recognize and appropriately treat a potential ectopic pregnancy and transport in a timely manner to
the most appropriate receiving facility. The clinical indicators which suggest the aim is being achieved
are the following:
1. Maintain and treat hemodynamic instability (tachycardia, pale, delayed capillary refill, hypotension,
weak peripheral pulse) with appropriate fluid resuscitation.
2. Pain control en route using inhalational or IV analgesics to achieve pain scale less than 4/10 or 3rd
face
3. Patient transported to most appropriate facility with pre-arrival notification, when required.
An ectopic pregnancy occurs when the conceptus implants and grows outside the endometrial/ uterine
cavity. May occur in the fallopian tubes, cervix, ovaries or abdominal cavity.
Initial assessment: As per CPG 1: Clinical Approach to the Adult Medical Patient and CPG 12: Clinical
Approach to the Obstetric Patient
Risk factors include: History of pelvic inflammatory disease, infertility or assisted conception and previ-
ous ectopic, Intrauterine Contraceptive Devices, Sexually Transmitted Diseases, endometriosis, pelvic
or tubal surgery and smoking.
Clinical Features: Pelvic or lower abdominal pain, usually unilateral, amenorrhea, vaginal bleeding,
heavy cramping and shoulder tip pain (Kehr’s sign)
1. Calm and reassurance to your patient and her family, it is likely she will be anxious with regards
to her condition. Consider that ANY female of reproductive age with PV bleeding or unexplained
lower abdominal or pelvic pain may be pregnant.
2. Allow the patient to assume a position of comfort, ensuring it doesn’t compromise their cardiovas-
cular stability.
3. Consider oxygen administration according to CPG 3.3, if deemed necessary.
4. Initiate IV therapy (large bore) en route to hospital:
 Hemodynamic instability may be indicative of a rupture ectopic with intraperitoneal haem-
orrhage. Administer IV fluids 250-500ml NS, if patient presents with signs and symptoms of
hemodynamic instability/ hypovolemic shock (pallor, tachycardia, delayed capillary refill, cold
and clammy skin, hypotension which may be associated with abdominal distention and/or ten-
derness/peritoneal signs).
 Reassess and repeat as necessary
 Consider establishing a second large bore IV, if significant bleeding or patient remains hemody-
namic unstable after initial fluid bolus of 500ml NS.
5. Consider appropriate analgesia according to CPG 6.1
6. Consider an anti-emetic (Ondansetron) to treat nausea and vomiting.
7. If PV bleeding is present provide sanitary pads to the patient and take all blood soaked items into
the ED – do not discard in the ambulance. This will assist in determining the volume of blood lost.
CPG 12.1.2
MANAGEMENT OF THREATENED
MISCARRIAGE
MANAGEMENT AIM
To provide women with a suspected, threatened miscarriage with supportive medical treatment and
transport to the closest most appropriate receiving facility. The clinical indicators which suggest the
aim is being achieved are the following:
face
3. Patient transported to most appropriate facility with pre-arrival notification, when required
Miscarriage is defined as the expulsion of the fetus at a stage when it is incapable with survival (be-
fore 20 weeks gestation but majority occur before 12 weeks)
Risk factors: Age, Stress, Maternal infection, Diabetic Mellitus, Smoking, Severe hypertension, Alcohol
consumption, Fibroids, Renal disease, Caffeine, Uterine dysfunction and untreated thyroid disease
Clinical Features: Vaginal Bleeding is the most common sign (may be heavy), Abdominal/pelvic pain
or period-like cramping, consider a septic abortion in the event that the patient present with fever,
severe pelvic pain, purulent discharge, and chills (medical emergency).
1. Initial assessment: As per CPG 1: Clinical Approach to the Adult Medical Patient & CPG 12: Clini-
cal Approach to the Obstetric Patient
2. Initiation IV therapy en route to hospital:
 Administer IV fluids 250-500ml NS, if patient presents with signs and symptoms of hemody-
namic instability/hypovolemic shock (pallor, tachycardia, delayed capillary refill, cold and clam-
my skin, hypotension).
 Reassess and repeat as necessary
4. If PV bleeding is occurring provide sanitary pads to the patient and take all blood soaked items into
the ED – do not discard in the ambulance. This will assist in determining the volume of blood lost.
CPG 12.1.3
MANAGEMENT OF PLACENTA
ABRUPTIO AND PREVIA
MANAGEMENT AIM
To recognize the signs and symptoms of Abruption and Previa Placenta and to provide appropriate
treatment and transport to the closest most appropriate receiving facility in a timely manner. The clini-
cal indicators which suggest the aim is being achieved are the following:
face.
ABRUPTIO PLACENTA:
Is defined as the premature separation of the placenta from the uterine wall before the delivery of the
fetus and should always be considered in the event of vaginal bleeding after 20 weeks of gestation.
Risk factors: age, recent trauma, Placenta Previa, previous abruption placenta, smoking, hyperten-
sion, pre-eclampsia, uterine infection and drug use.
Clinical features: vaginal bleeding (bleeding may be concealed), abdominal tenderness and/or disten-
tion, uterine tenderness and painful contractions, decreased fetal movement, signs and symptoms of
hypovolemic shock.
PLACENTA PREVIA:
Placenta implants in the lower uterine segment and can be classified according to location. Placenta
Previa should always be considered in the event of vaginal bleeding after 20 weeks gestation.
Risk factors: advanced age, multiple gestations, fertility treatment, previous uterine surgery, short
interpregnancy interval trauma, smoking, previous caesarean section and drug use.
Clinical features: Painless vaginal bleeding, usually bright red of variable amounts, uterine tenderness
unlikely, may present with signs and symptoms of hypovolemic shock if severe haemorrhage.
1. Initial assessment: As per CPG 1: Clinical Approach to the Adult Medical Patient and CPG 12 Clini-
2. Initiation IV therapy (large bore) enroute to hospital:
 Administer IV fluids 250-500ml NS, if patient presents with signs and symptoms of haemo-
dynamic instability/ hypovolemic shock (pallor, tachycardia, delayed capillary refill, cold and
clammy skin, hypotension).
 Administer TXA 1g IV over 5-10 minutes.
 Consider establishing a second large bore IV, if significant bleeding or patient remains haemo-
dynamically unstable after initial fluid bolus (500ml NS).
4. If PV loss is occurring provide sanitary pads to the patient and take all blood soaked items into the
ED – do not discard in the ambulance. This will assist in determining the volume of blood lost.
CPG 12.1.4 MANAGEMENT OF PRE-TERM LABOUR
 Gestation between 24 - 34 weeks?  Braxton-Hicks contractions

 Painful contractions 30 seconds long,  Placenta abruption
> 3 in 30 minutes?  GIT pain (appendicitis)
 No contra-indication?
 Consider analgesia: Penthrox 3ml inhalation

 Analgesia: IV Paracetamol: 1g IV over 20 minutes
AP & CCP
CPG 12.1.4
MANAGEMENT OF PRE-TERM LABOUR
MANAGEMENT AIM
To recognize the signs and symptoms of pre-term labour and to provide appropriate treatment and
transport to the most appropriate receiving facility in a timely manner, without causing unnecessary
distress to the mother. The clinical indicators which suggest the aim is being achieved are the follow-
ing:
1. Timely diagnosis of pre-term labour.
2. Provide prophylactic pharmacologic therapy to prolong gestation and reduce the incidence of Re-
spiratory Distress Syndrome (RDS) and infection.
1. Pre-term Labour is uterine contractions of sufficient frequency and intensity to effect progressive
effacement and dilation of the cervix, after 20 weeks of gestation but prior to 37 weeks gestation.
2. Risk factors: PROM, multiple pregnancies, assisted conception, infection, trauma, stress, incom-
petent cervix, obstetric complications (maternal hypertension, fetal abnormalities and previous
miscarriages.
3. Clinical features: Regular, persistent, painful contractions, Spontaneous rupture of membranes,
Bleeding “show” or bloody discharge, persistent, low backache
2. Consider appropriate analgesia: Pain can be managed with Penthrox and/or IV Paracetamol. Both
Penthrox and IV Paracetamol are acceptable forms of analgesia in the intrapartum phase of labour
(narcotics are contraindicated in late second stage labour).
CPG 12.2 MANAGEMENT OF PRE-ECLAMPSIA AND ECLAMPSIA
 Hypertension >SBP 140/90 diastolic  Chronic hypertension

 Visual disturbance/ change in LOC,  Gestational hypertension
headaches?  Epilepsy
 Oedema?
 RUQ tenderness?
 Do not allow patient to walk

 Establish IV but restrict fluids (<80ml/hr)
 Request CCP assistance
PRE-ECLAMPSIA
* Monitor patient and transport to hospital.
* Magnesium is not recommended solely as an anti-hypertensive agent.
* If pre-eclampsia is suspected, administer Magnesium 4g in 100ml NaCl
- infuse over 10 minutes IV/IO
* If signs of magnesium toxicity are identified, stop infusion and administer
Calcium Chloride 1g over 10 minutes.
ECLAMPSIA
(Active seizure or postictal)
 Magnesium: 4g in 100ml NaCl – infuse over 10 minutes IV/IO. This
is the definitive treatment to stop seizures as well as prevent further
seizures.
 Midazolam: In status seizure if magnesium is contra-indicated, unavail-
able, or ineffective. Administer as per CPG 5.2: Adult seizures (page 82 )
 If signs of magnesium toxicity, Calcium Chloride 1g over 10 minutes
 Transport Priority 2 (if P1 required – DO NOT USE SIRENS, as it may

precipitate seizures)
AP & CCP CCP
CPG 12.2
MANAGEMENT OF PRE-ECLAMPSIA
AND ECLAMPSIA
MANAGEMENT AIM
To recognize and appropriately treat pre-eclampsia and eclampsia with transport in a timely manner
to the closest most appropriate receiving facility. The clinical indicators which suggest the aim is being
1. To recognize and treat patient presenting with pre-eclampsia.
2. To recognize eclampsia and treat/prevent further eclamptic fit with magnesium sulphate
3. To transport the patient to an appropriate facility in a safe and expedient manner with pre-notifica-
tion
SEVERE PRE-ECLAMPSIA:
A patient more than 20 weeks pregnant with a blood pressure of _ > 140 systolic and/or _
> 90mmHg
diastolic with more than one of the following clinical features:
1. CNS:
 Visual Disturbances: Flashing lights, blurred vision and blindness

 Altered mental status (including confusion to decreased LOC)
 Severe headaches
 Hyperreflexia and/or clonus (>3 beats) is a sign of cerebral irritability
2. Liver:
 Nausea and vomiting
 Epigastric/RUQ tenderness is a sign of liver involvement
3. Cardiovascular:
 Facial oedema
 Pulmonary oedema
4. Uterine tenderness or vaginal bleeding from placental abruption
5. Other haematological, hepatic or renal derangement cannot be assessed in the pre-hospital set-
ting.
6. Eclampsia:
 One or more generalized seizures associated with pre-eclampsia in patient >20 weeks gesta-
tion
RECOMMENDATIONS FOR BP MEASUREMENTS:

1. When possible, the BP should be measured with the patient in a sitting position with the arm at
the level of the heart.
2. Use an appropriately sized BP cuff.
3. Consider comparing automated BP reading with a mercury sphygmomanometer reading as auto-
mated blood pressure monitors may over or underestimate readings.
2. Do not allow the patient to walk.
3. Indication for Magnesium Sulphate administration in pre-eclampsia and eclampsia:
 Magnesium is not recommended solely as an antihypertensive agent.
 Recommended treatment for the prevention of eclampsia in patients with severe pre-eclampsia
(see treatment recommendations below)
 Recommended as the first line treatment of eclampsia and the presentation of further seizures
(see treatment recommendations below)
Pre-eclampsia:
 Administer Magnesium Sulphate infusion: 4g in 100ml NaCl - infuse over 10 minutes IV/IO
Eclampsia: (seizures are commonly short-lasting and terminate spontaneously)
 Open, clear and protect airway – place patient in lateral position (if after 20 weeks gestation
use left lateral position)
 Initiate oxygen therapy (CPG 3.3) - supplemental oxygen via NRB or BVMR as necessary to
maintain a SpO2 of ≥ 95%.
 If advanced airway management is required this should be done using careful sedation, paraly-
sis and LT.
 Risk of regurgitation and aspiration can be reduced by transporting the patient in the lateral
position.
 Anticipate a difficult airway in pregnancy and plan appropriately: Upper airway physiological
changes in pregnancy include hyperaemia, oedema and hypersecretion which may impair visu-
alization and increase the possibility for bleeding during airway manipulation.
 Restrict fluid administration due to the risk of pulmonary oedema.
 Active seizures: Administer Magnesium
 Patient post-ictal: Consider the administration of Magnesium to prevent further seizure.
 Midazolam should not be used for eclampsia prophylaxis or treatment, unless Magnesium is
contraindicated, unavailable or ineffective or IV/IO access failed. Consider Midazolam IN or IM
(IV access failed) or IV/IO if Magnesium is contraindicated, unavailable or ineffective, or if the
diagnosis is uncertain (Epilepsy associated with pregnancy).
 If an epileptic patient is having a seizure after 20 weeks of pregnancy and has a history of
hypertension or pre-eclampsia, treat for eclampsia. If there is no hypertension or history of
pre-eclampsia treat for epilepsy. Monitor blood pressure until after the post-ictal phase.
 Closely monitor vital signs (BP, HR, RR and SpO2 every 15 minutes) and monitor for signs of
magnesium toxicity:
» Nausea, hot flushes, weakness
» Slurred speech/ Confusion/ Blurred vision
» Loss of Deep Tendon Reflexes/ Absent patellar reflexes
» Hypotension/ Pulse oximetry <95%
» Respiratory depression and respiratory arrest
» Cardiac arrhythmia/ ECG changes (e.g. widened QRS complex, increased PR interval,
prolonged QT interval, heart block)
» Chest pains
In the event of signs of Magnesium toxicity – stop infusion. If stopping Magnesium infusion is not suffi-
cient consider Calcium Chloride IV slowly over 10 minutes.
CPG 12.3
MANAGEMENT OF DELIVERY AND

ASSOCIATED COMPLICATIONS
CPG 12.3.1
MANAGEMENT OF IMMINENT DELIVERY

OF THE NEWBORN
MANAGEMENT AIM
To recognize imminent delivery and to ensure the safe delivery of a neonate in the field, where appro-
priate. To identify clinical factors which indicate resuscitation of the newborn is necessary. To provide
appropriate care of the mother and deliver of the placenta, as required. Knowledge of the following
aspects will facilitate this process:
1. Diagnosis of labour at the first, second and third stages.
2. Providing pain management (CPG 6.1) during the labour process.
3. Identifying any complications that arise during the 3 stages of labour and managing appropriately
4. Delivery of the newborn in a safe manner.
5. Assessing the APGAR of the newborn and provide resuscitation where required.
6. Transport of mother and newborn in a timely manner to the closest most appropriate receiving
facility with pre-notification.
THREE STAGES OF LABOUR:

1st Stage: Regular contractions of the uterus and full dilation of the cervix.
2nd Stage: Commences when the cervix is completely dilated and concludes when the newborn is
delivered.
3rd Stage: Delivery of the placenta.
SIGNS AND SYMPTOMS OF 2ND STAGE OF LABOUR:
 Active pushing/ grunting
 Bulging membranes
 Strong contractions (longer duration with short intervals between)
 Rectal pressure
 Bulging perineum
 Urge to push
 Crowning - presenting part visible
 Mother becomes irrational
SIGNS OF PLACENTAL SEPARATION:

 Lengthening of the cord
 Uterus becomes firmer
 Gush of blood
2. Consider supplemental oxygen as per CPG 3.3, particularly, in the event that there is any indica-
tion of fetal distress (meconium stain liquor) or delivery complications (prolonged second stage).
3. Consider appropriate analgesia: Pain can be managed with Penthrox and/or IV Paracetamol. Both
4. Prepare for imminent delivery and the possibility of neonatal resuscitation.
5. When the head is on view, apply light pressure to the perineum with gauze, to reduce the chance
of tearing.
6. Ask the mother to “pant” during delivery of the baby’s head – you want to avoid explosive delivery
of the head by placing one hand gently on the presenting part of the head to ensure it emerges
smoothly.
7. Once the head is delivered, it will turn (restitute) towards one side. Support the baby’s head and
finger sweep around the neck to check for the presence of the cord. If the cord is around the ba-
by’s neck – slide your finger under the cord and loop it back over the baby’s head.
8. With the next contraction, deliver the anterior shoulder by supporting the baby in a downwards
position. Then deliver the posterior shoulder by supporting the baby in an upwards direction.
9. The baby’s body should follow with little resistance.
10. Record the time of the birth.
11. Wrap the baby in a towel and stimulate it by rubbing the back or flicking the soles of the feet.
12. Suction is not usually required – if suction is required (CPG 13.1), suction the mouth first and then
each nostril. Be very careful as the baby’s airway is delicate.
13. Record the baby’s APGAR at 1 and 5 minute intervals.
14. Cord management:
 Delayed clamping is defined as cord clamping between 30 seconds to three minutes after birth.
 Do not clamp or cut the cord, unless the infant requires earlier intervention (positive pressure
ventilation), the recommendation is to wait for 60 seconds then clamp the cord. Keep the new-
born below the level of the placenta to allow gravity to transfuse blood through the cord.
 Place the first clamp approximately 10-15cm from the newborn’s umbilicus. Then place a sec-
ond about 5cm further, clamp after the segment between the 2 clamps has been milked. The
cord can then be cut in a relatively bloodless manner.
15. If resuscitation of the newborn is required, refer to CPG 13.1 (Care and Resuscitation of the new-
born).
16. Placental delivery:
 NB: Do not apply traction to the cord in order to deliver. Rotate or twist the placenta and the
membranes in a circular motion to ensure complete delivery – this ensures the membranes
are not torn which can result in retained products of conception. The placenta and membranes
should be placed in a bag/ container to be examined later at the hospital. The abdomen can be
palpated lightly to ensure the uterus has contracted.
CPG 12.3.2
MANAGEMENT OF BREECH
PRESENTATION
MANAGEMENT AIM
To identify a breech presentation through effective questioning of the mother and effectively delivers
the newborn safely. To recognize when breech delivery is imminent delivery and anticipate the need
for resuscitation of the newborn. To provide appropriate care of the mother and delivery of the placen-
ta, as required. Knowledge of the following aspects will facilitate this process:
1. Identify the presenting part (non-cephalic), when delivery is imminent.
2. Providing appropriate analgesia: Pain can be managed with Penthrox and/or IV Paracetamol. Both
3. Identifying any complications
4. Delivery of the newborn through the assisted vaginal breech delivery.
5. Assessing the APGAR of the newborn and provide resuscitation where required.
Breech presentation occurs when the fetus enters the birth canal with buttocks or feet first, (compared
with a cephalic presentation where the head presents first). The buttocks and feet do not provide an
effective wedge to block and dilate the cervix. As a result the umbilical cord may prolapse and the
head can get trapped during the delivery.
Complications associated with vaginal breech deliveries:
 Low APGAR score due to fetal hypoxia from umbilical cord compression
 Fetal head entrapment
 Nuchal arms - arms wrapped around back of neck
 Cervical spine or other injuries to newborn
 Umbilical cord prolapse
2. Initiate IV therapy enroute to hospital. Do not delay assisting with imminent delivery to initiate IV.
3. If delivery is imminent, transport without delay, whilst keeping the mother comfortable and calm.
4. Prepare for imminent delivery and the possibility of neonatal resuscitation equipment enroute.
5. Do not place the mother in a supine position as the weight of the uterus and baby can impede re-
turn of blood from the inferior vena cava. Place a towel under the mother’s right buttock to elevate
her approximately 15 degrees.
6. Consider supplemental oxygen as per CPG 3.3, particularly, in the event that there is any indica-
tion of fetal distress (meconium stain liquor) or delivery complications (prolonged second stage)
7. If delivery occurs in the ambulance, do not provide traction to the baby. Assist delivery of the foetus
using the “assisted vaginal breech delivery”. This is where the foetus delivers spontaneously up to
the umbilicus – whereby the paramedic supports delivery of the legs, buttocks and torso. Manoeu-
vres are then initiated to assist with delivery of the rest of the body, the arms and the head.
8. In a footling / buttock breech, allow the baby to deliver spontaneously to the level of the umbilicus.
DO NOT pull on the feet – this may precipitate head entrapment in an incompletely dilated cervix,
or may precipitate nuchal arms.
9. Leave the fetal membranes intact for as long as possible. This will prevent cord prolapse and act
as a dilating wedge.
10. Once the fetal umbilicus is past the perineum, gentle downwards and outwards traction of the foe-
tus until the scapula are visible – this pressure should coincide with the mother’s contractions.
11. If possible, ask an assistant to apply transfundal pressure from above to keep the head flexed.
ASSISTED VAGINAL BREECH DELIVERY:
Figure 1 and 2: The Ritgen manoeuvre is applied to take pressure off the perineum during vaginal delivery. The Ritgen
manoeuvre is the delivery of the infant’s head while applying pressure on the perineum and controlling the speed of
delivery by applying gentle pressure to the presenting part with the other hand.
Figure 3: With a towel wrapped around the fetal hips, gentle downward and outward traction is applied in conjunction
with maternal expulsive efforts until the scapula is reached.
12. If nuchal arms present, rotate the infant so the fetal face turns towards the maternal symphysis
pubis. Then assist the delivery of each arm in turn before delivering the head:
13. Rotate the infant 90 degrees and gently sweep the anterior arm out of the vagina by pressing on
the inner aspect of the arm or elbow and sweeping the arm across the infant’s chest.
14. Rotate the foetus 180 degrees in the reverse direction and sweep the other arm out of the vagina
– then rotate back 90 degrees to the original position.
15. Maintain the fetal head in the flexed position during delivery to allow passage of the smallest di-
ameter of the head. This is most effectively done utilizing the Mauriceau-Smellie-Veit manoeuvre.
Support the foetus on the right forearm. Press with the middle finger of the right hand on the fetal
chin and place the index finger and ring finger on either side of the malar eminences to promote
head flexion while counter pressure is applied to the fetal occiput with the left arm posterior to
further encourage flexion. An assistant should apply suprapubic pressure to assist in head flexion.
The fetal body is held in the neutral position to avoid overextending the neck.
Figure 5: Mauriceau Smellie Veit maneuver
16. During delivery of the head, avoid extreme elevation of the body – this can result in hyperexten-
sion of the cervical spine and can result in potential neurological injury.
17. Once the fetus is completely delivered, refer to CPG 13.1 – Care of the newborn
CPG 12.3.3
MANAGEMENT OF UMBILICAL CORD

PROLAPSE
MANAGEMENT AIM
To identify and appropriately treat an umbilical cord prolapse and to recognize when delivery is im-
minent delivery. To anticipate and prepare for resuscitation of the newborn. To provide appropriate
care to the mother and delivery of the placenta, as required. Knowledge of the following aspects will
facilitate this process:
1. Identify the presenting part, when delivery is imminent
2. To perform skills to minimize foetal harm
3. Providing appropriate analgesia: Pain can be managed with Penthrox and/or IV Paracetamol. Both
4. Prepare for neonatal resuscitation and assessing the APGAR of the newborn where required.
2. Safe and rapid transport to an appropriate facility that can perform an emergency caesarean sec-
tion with pre-notification.
3. Administer supplemental oxygen as per CPG 3.3.
4. First stage of labour:
 If the cord is still pulsating and no pressure is being applied to it from the presenting part, cover
the cord in wet gauze (use warm sterile saline) and do not handle too much.
» If the presenting part is applying pressure to the cord, and the cord is subsequently not
pulsating. Aim to reduce the risk of cord compression by elevating presenting part:
» Position: Place mother in a deep knee chest position or head down and feet up (Trendelen-
burg position) or placing pillow under left hip (aggravated Sims position)
Figure 1: Aggravated Sims Position

» Manually elevating the presenting part: Insert sterile gloved fingers into the vagina to ele-
vate the presenting part away from the cord and allow circulation to resume to the foetus.
Avoid excessive handling of the cord. DO NOT REMOVE YOUR HAND UNTIL IN THE
DELIVERY SUITE/ OPERATING THEATRE.
5. If delivery is imminent, undertake procedural stop and deliver immediately (see SOP 4.8 I)
6. Prepare for resuscitation of the newborn
CPG 12.4
MANAGEMENT OF POST DELIVERY (OR

3RD STAGE) COMPLICATIONS
MANAGEMENT AIM
Is to recognize and appropriately treat post-delivery or 3rd stage complications and transportation of
the patient in a timely manner to the closest most appropriate receiving facility, with pre-notification.
1. To identify and treat postpartum haemorrhage
2. To identify and treat retained placenta
3. To identify and treat uterine inversion
4. To monitor the patient’s vital signs and correctly identify a decompensating patient
5. To appropriately care for the newborn infant
6. To transport the patient in a safe and expedient manner to an appropriate facility
PPH DEFINITIONS:
 Primary PPH is defined as blood loss of 500-1000ml from the genital tract occurs within 24
hours of delivery.
 Severe Primary PPH defined as blood loss of more than 1000ml from the genital tract occurs
within 24 hours.
RETAINED PLACENTA:
Placenta not expelled within 30 minutes of the start of the 3rd stage of labour.
4 T’S OF PPH:
 Tone: Uterine atony or uterine abnormality
 Tissue: retained portion of the placenta preventing effective contraction
 Trauma: Damage to genital tract, uterine rupture, prolonged labour or vaginal/cervical lacera-
tion
 Thrombosis: Clotting abnormalities
 Other causes: Uterine infection, hypertensive disorders, magnesium sulfate use, inducted la-
bour, large baby, previous PPH
UTERINE INVERSION:
Uterine inversion is a rare life-threatening obstetric emergency when the uterus invert in various de-
grees.
SEVERITY:
 1st degree: Uterus partially inverted
 2nd degree: Fundus has passed through the cervix but not outside vagina,
 3rd degree: Fundus is prolapsed outside the vagina,
 4th degree: Uterus, cervix and vagina are completely turned inside out and are visible
TIME:
 Acute: Within 24 hours of birth
 Sub-acute: Between 24 hours and 30 days postpartum
 Chronic: Within 30 days postpartum
RISK FACTORS:
 Aggressive management of 3rd stages of labour for example excessive fundus massaging and
cord traction
 Fundal placement of placenta
 Abnormal adherenced placenta
 Nulliparity
 Without a known cause
 Antepartum use of MgSO4
2. Initiate IV therapy. Administer IV fluids 250-500ml NS, if patient presents with signs and symptoms
of hemodynamic instability/ hypovolemic shock (pallor, tachycardia, delayed capillary refill, cold
and clammy skin, hypotension).
3. Provide the patient with sanitary pads and take all blood stained items to hospital with the patient.
4. Consider appropriate analgesia according to CPG 6.1:
5. Notify the receiving facility early as surgery may be required or a blood transfusion may be re-
quired
6. Transport to the closest most appropriate medical facility. In the event of severe haemorrhage with
hemodynamic instability transport priority 1 and pre-notify.
POST PARTUM HAEMORRHAGE

7. If the fundus is boggy (uterine atony – poor contraction)
 Massage fundus until firm and blood loss reduces
 Use a cupped hand and apply firm pressure in a circular motion
 If possible, encourage the mother to empty her bladder
 Encourage the baby to suckle the breast
8. If the fundus is firm:
 Administer IV fluids 250-500ml NS, if patient presents with signs and symptoms of hemody-
namic instability/hypovolemic shock (pallor, tachycardia, delayed capillary refill, cold and clam-
my skin, hypotension).
 Reassess and repeat as necessary.
 Administer TXA 1g IV over 5-10 minutes.
 Manage any visible lacerations with a dressing and firm pressure
9. NB: Rapid recognition of PPH is essential to successful management. The major factor in the
adverse outcomes associated with severe haemorrhage is a delay in initiating appropriate man-
agement.
RETAINED PLACENTA:
10. Do not apply traction to the umbilical cord
11. Massage fundus until firm - Use a cupped hand and apply firm pressure in a circular motion to
encourage contraction
12. If possible, encourage the mother to empty her bladder
13. Encourage the baby to suckle the breast
UTERINE INVERSION
14. Cover and protect exposed uterus with moist sterile dressings
15. Do not attempt to remove the placenta or attempt to replace the inverted uterus
CPG 12.5
MANAGEMENT OF MATERNAL CARDIAC

ARREST
MANAGEMENT AIM
To identify cardiac arrest with appropriate modifications of standard cardiac arrest and to immediate-
ly initiate intervention to restore perfusion to the brain and other organs and terminate resuscitation
when appropriate interventions have failed to achieve any result or after return of spontaneous circula-
tion. The clinical indicators which suggest the aim is being achieved are the following:
the latest international guidelines on resuscitation.
4. Advanced Cardiac Life Support and post cardiac arrest therapy to prevent reoccurrence of cardiac
arrest.
1. Initial assessment: As per CPG 1: Clinical Approach to the Adult Medical Patient
2. Undertake resuscitation as per CPG 4.1, in addition:
3. Optimize maternal cardiac arrest management by considering physiological changes:
 Anticipate a difficult airway:
» Upper airway physiological changes in pregnancy and include hyperaemia, oedema and
hypersecretion. These changes may impair visualization and increase the possibility for
bleeding during airway manipulation.
» Failed intubation is a major cause of maternal mortality.
» Placement of a supraglottic airway is expectable.
» Endotracheal intubation should be undertaken by an experience practitioner utilizing no
more than 2 attempts. Prepare a second ET tube one size smaller than the expected size.
» If the placement of an advanced airway fail, optimize ventilation with BVMR and 100%
oxygen
 Due to reduced functional residual capacity and increased oxygen demand in pregnancy, hy-
poxia develops rapidly. Optimizing ventilation (BVMR) with a 100% of oxygen is important.
 Relieve aortocaval compression during chest compressions to improve venous return and
chest output: Perform manual left lateral uterine displacement. If manual displacement cannot
be performed or maintained, place the patient a left lateral tilt of 15 to 30 degrees.
Figure 1: Left uterine displacement with 2-handed technique
Figure 2: Left uterine displacement using 1-handed technique
4. Perform chest compressions in a slightly higher position than normal on the sternum. The use of
the LUCAS II is not recommended. Place the patient supine and deliver high quality compression.
The uterus should be displaced manually (as per figure 1 and 2 above).
5. Start IV therapy above the diaphragm (upper extremities) and assess hemodynamic status. Ad-
minister fluid boluses as needed.
6. Consider reversible causes of cardiac arrest in pregnant patients in order to target management.
7. Use the recommended drug and defibrillation dosages as for standard adult cardiac arrest (CPG
4.1). Place the lower debrillation pad under the breast tissue.
8. Consider Magnesium toxicity as a cause of maternal cardiac arrest – stop infusion and/or adminis-
ter Calcium Chloride IV.
9. Consider the possibility of emergency caesarean section preformed in-hospital. Transport the
patient promptly to the closest most appropriate facility and pre-notify the facility. Apply the LUCAS
for ongoing compressions during transport.
10. Post cardiac arrest sedation - Should not be done routinely, unless there is a risk of self-injury or a
requirement to facilitate improved ventilator compliance.
CPG 12.6
MANAGEMENT OF OBSTETRIC TRAUMA
MANAGEMENT AIM
Optimal management of the pregnant trauma patient requires a coordinated, comprehensive and
multidisciplinary approach, whereby the Ambulance Service provides the initial pre-hospital interven-
tions and timely transport to an appropriate facility. Clinical indicators which suggest the aim is being
1. Understanding how the anatomical and physiology of pregnancy will alter the response to injuries
and provide appropriate treatment accordingly.
2. Ensuring the appropriate assessment and resuscitation of the mother ensures the resuscitation of
the foetus.
3. Pain control enroute using inhalational or IV analgesics to achieve pain scale less than 4/10 or 3rd
face.
4. Ensure appropriate positioning during transportation to prevent the effects of supine hypotension
syndrome.
Take an appropriate medical and obstetric history and conduct physical assessment to identify inju-
ries. The best initial treatment for the fetus is the provision of optimal resuscitation of the mother.
1. Initial assessment: As per CPG 9: Clinical Approach to the Adult Trauma Patient.
2. Always administer high-flow supplemental oxygen, because the pregnant patient is less able to
compensate for hypoxia. Similarly, consider early endotracheal intubation to ensure optimal oxy-
genation and ventilation. Anticipate and prepare for a difficult airway and rapid desaturation sec-
ondary to the anatomical and physiological changes of pregnancy.
3. Control obvious bleeding and identify any possible occult and/or vaginal bleeding. Due to the
anatomical and physiological changes in pregnancy, hypovolaemia should be anticipated and fluid
resuscitation initiated early. Establish intravenous access using large-bore cannulae and provide
isotonic fluid resuscitation, as required. Consider intravenous access en-route to hospital in case
of uncontrollable haemorrhage.
4. For pregnant patients at >20 weeks gestation who need spinal motion restriction, the uterus should
be displaced manually to the left side to relieve pressure on the IVC. If this is unsuccessful, place
a wedge under the right hip area, tilting the patient approximately 30º towards her left side.
6. Treat all other injuries identified as recommended in CPG 9.1 – CPG 9.9
CPG 13
CLINICAL APPROACH TO THE

PAEDIATRIC PATIENT
Paediatric patients are anatomically, physiologically and psychologically different to adults. These
differences play an important role in communication, assessing and treating paediatric patients. Prac-
titioners must consider these differences during the assessment and treatment of critically ill or injured
paediatrics.
ANATOMICAL AND PHYSIOLOGICAL DIFFERENCES:
AIRWAY:
Hypoxia and inadequate ventilation is the most common cause of cardiopulmonary arrest in pediatrics,
as a result effective airway management is paramount.
Paediatrics have a smaller airway diameter and the larynx is located in a more anterior and superi-
or position. Their tongue is also larger in proportion to their mouth than that of an adult. All of these
factors predispose them to airway obstruction and any slight narrowing of the airway significantly
increases their work of breathing. The head of a paediatric is larger in relation to their body size with a
short neck and prominent occiput, predisposing them to head injuries as well as increasing the risk of
airway occlusion by hyperflexion. It is important to place padding under the child’s shoulders to open
the airway (neutral position).
The respiratory system is underdeveloped. Babies are obligatory nose breathers. Babies and small
children breath mainly with their diaphragm as the intercostals muscle and ribs are too pliable to
support ventilation. The work of breathing consumes 15% of oxygen and the respiratory muscles are
easily fatigued.
The circulating blood volume (80-90 ml/kg) of children is higher per kilogram than adults (70 ml/kg)
but their absolute blood volume is small due to small body size. Their cardiovascular system is able
to compensate better for blood loss, hypotension develops late and is a pre-terminal sign. Paediatrics
have a limited ability to increase stroke volume therefore cardiac output is heart rate dependent. Bra-
dycardia is commonly associated with hypoxia and is a very ominous sign.
The bone structure is softer due to incomplete calcification and bones being more cartilaginous. Thus
greenstick fractures (incomplete) are more common. This also predisposes them to internal injuries
(for example pulmonary contusions without rib fractures) as the bones bend rather than absorbing
force.
In smaller children the abdominal organs are relatively large in relation to the rib cage thus they are
not fully protected making them more prone to liver and spleen injuries from blunt force trauma.
Mechanism of injury will cause different injuries to children due to their size and altered center of grav-
ity. Children are more prone to domestic and playground injuries as they are less aware of dangers
and more likely to take risks.
NORMAL VITAL SIGN RANGE FOR PAEDIATRIC PATIENTS
Age group Resp rate Heart rate Systolic BP Temperature RBS

Term baby 40-60 100-170 50 36.5 2.6-6mmol/L
3 months 30-50 100-170 50 36.5 4-6mmol/L
6 months 30-50 100-170 60 36.5 4-6mmol/L
1 year 30-40 110-160 70-90 36.5 4-6mmol/L
1-2 year 25-35 100-150 80-95 36.5 4-6mmol/L
2-5 year 25-30 95-140 80-100 36.5 4-6mmol/L
5-12 year 20-25 80-120 90-110 36.5 4-6mmol/L
>12 year 15-20 60-100 100-120 36-37.6 4-6mmol/L
ESTIMATE WEIGHT CALCULATIONS:

0 - 12 Months: (age x 0.5) + 4
1 - 5 years: (age x 2) + 8
6 - 14 years: (age x 3) + 7
Circulating blood volume for paediatrics: 80 – 85 ml/kg
RESPONDER SAFETY
1. Standard and Environmental Precautions (see SOP 2.1)
2. Observe for any dangers (dangers to crew, patient, bystanders)
PAEDIATRIC ASSESSMENT:
The assessment of critically ill and injured paediatric patients is often challenging, in particular if en-
counters with paediatrics are infrequent.
The assessment involves the following:
 Paediatric Assessment Triangle including the primary survey
 Secondary Survey:
» Focused history
» Detailed physical examination and vital signs assessment
 Ongoing assessment
The paediatric assessment triangle is a standardized tool for the emergency assessment of critical ill
and injured paediatrics of all ages. The assessment triangle is intended to be a quick initial assess-
ment conducted in 60 seconds and requires no equipment. The triangle includes three distinctive
sequential assessment steps: appearance, work of breathing and circulation assessment.
Appearance: The general appearance of a pediatric patient is the most important factor in the assess-
ment of a critical illness or injury. It reflects the adequacy of ventilation, oxygenation, brain perfusion
and central nervous system function. It includes assessing the child mental status, muscle tone and
identifying whether the child appears critically ill. The component of appearance can be assessing by
using the mnemonic TICLS:
T - Tone: Is the child active, listless or lethargic? Is the child moving spontaneously, sitting or
standing as appropriate for age or supporting the weight of their head?
I - Interactivity: Does the child interact with you or their parents or caregiver? Are you able to
gain the child’s interest or engage them in play or activity? Does the child react to
sounds?
C - Consolability: Can the child be comforted by their parents or caregiver? Is the child behaving to
external stimuli as you would predict?
L - Look/gaze: Are the child and infant able to fix their gaze on his parents, caregiver or the clini-
cian?
S - Speech/cry: Is the child using speech appropriate for age, do the child or infant have a strong
and vigorous or weak cry?
ASSESS WORK OF BREATHING:
 Look for abnormal positioning:
» Head bobbing, tripod position and/ or sniffing position.
 Listen for abnormal audible breath sounds (snoring, stridor, wheezing, grunting and hoarse
voice):
» Snoring, hoarse and/ or muffled voice, difficulty swallowing and/ or stridor suggest upper
airway obstruction caused by infection, swelling and foreign body airway obstruction. Stri-
dor is an abnormal high pitched sound caused by turbulent airway flow through a partially
obstructed upper airway (extra thoracic airways).
» Wheezes: High pitched expiratory sound causes by turbulent airway flow through the ob-
struction or narrowing of the intrathoracic airways.
» Grunting is an audible expiratory noise produced by an effort to prevent airway collapse by
generating positive end-expiratory pressure (PEEP)
 Look for visual signs on increased work of breathing (retractions, tachypnea, tracheal tugging,
abdominal breathing and nasal flaring):
» Tachypnea: Increased respiratory rate is an important sign of illness in young children.
» Retractions may occur in several areas of the chest and indicates respiratory distress and
an increased use of muscles to breathe. Examples: intercostal (between ribs), subcostal
(below rib cage) or suprasternal (above sternum).
» Abdominal breathing is the use of abdominal muscles to breathing causing a see-saw
movement of the chest wall and abdomen during respiration
» Nasal flaring is the widening of the nostrils during inspiration. In infants and children, nasal
flaring indicate respiratory distress.
 Are airway, oxygenation and ventilation adequately maintained and clear? Is the child in respi-
ratory distress? Are the airway obstructed?
ASSESS CIRCULATION:
 Assess the pulse rate and volume:
» Infants and small children have a limited ability to increase stroke volume and as a result
cardiac output is very dependent on heart rate. Tachycardia is an early sign of shock and
bradycardia is an ominous sign of significant hypoxia or acidosis.
 Assess skin color and mucous membrane (pallor, mottling, cyanosis and petechiae):
» Mottling: Patchy discoloration of the skin caused by poor perfusion and vasoconstriction.
 Assess skin turgor:
» Skin turgor is the degree of skin elasticity and poor skin turgor is a clinical indication of
dehydration. Skin turgor is assessed by pinching a portion of skin between two fingers
for a few seconds (5 seconds) before releasing and observing the time it takes to return
to a normal position (within 2 seconds) In infants and small children skin turgor should be
assessed on the abdomen near the umbilicus.
 Assess capillary refill:
» Capillary refill can be assessed on the nailbed, forehead or heel of the foot.
» Raise the extremity above the heart, press gently over a finger’s nailbed, forehead of heel
to blanch the skin and occlusion of blood flow. Release pressure and count the time it
takes for a full return of blood to the blanched tissue. Normal capillary refill time is less than
2 seconds. Delayed capillary refill indicates poor blood flow.
 Is circulation (cardiac output and perfusion) adequate?
SECONDARY SURVEY:
 Focused history:
» Ascertain the chief complaint or mechanism of injury in trauma from child if possible, other-
wise from the parents or guardian.
(Chief complaint: The chief complaint is the main reason the person called for the ambu-
lance. It may not actually be the primary cause of the problem but merely a secondary
symptom (like seizures in pyrexia). It should give you a good starting point for the prob-
lem-focused history).
» Begin simultaneous process of asking a problem focused history:
Brief Problem Focused History: This is focused initially on the chief complaint and any sus-
picions that flow from the chief complaint.
 Use a structured system (eg. SAMPLE)
 Consider possible differential diagnoses of chief complaint and focus your questions to
include or exclude various conditions.
 Use questions to rapidly identify any potentially life threatening problems so treatment
can be initiated rapidly.
» Detailed physical examination and vital signs assessment
In the medical patient the specific problem focused assessment depends on the condition
present. In general the following are important:
 Measure all vital signs, RBS and age appropriate Glasgow Coma Score (GCS)
Assessment Area Infants (0 – 12 months) Children Score
Eye Opening Open Spontaneously Open Spontaneously 4

Open in response to verbal Open in response to verbal 3
stimuli stimuli
Open in response to pain Open in response to pain only 2
only
No response No response 1
Verbal Response Coos and babbles Oriented, appropriate 5
Irritable cries Confused 4
Cries in response to pain Inappropriate words 3
Moans in response to pain Incomprehensible words 2
Motor Response Moves spontaneously and Obeys commands 6
purposefully
Withdraws to touch Localizes painful stimulus 5
Withdraws in response to Withdraws in response to pain 4
pain
Responds to pain with de- Responds to pain with flexion 3
corticate posturing (abnormal
flexion)
Responds to pain with decer- Responds to pain with extension 2
ebrate posturing (abnormal
extension)
» Undertake a pain assessment (if pain present use FLACC Scale – CPG 13.11)
» Assess the relevant parts of these various systems based on patient chief complaint and
brief focused history.
 Head and neck: AVPU, pupil size and reaction speed, unusual breath odours. Assess
fontanelle in infants (sunken or bulging), absence of tears and dry mucous membranes
(mouth).
 Chest (inspect, palpate, auscultate and percuss): Abnormal movement symmetry,
breath sounds on auscultation (normal, wheezing, crackles or absent), use of accesso-
ry muscles of the upper chest, neck and abdomen. Presence of cough.
 Abdomen: Rigidity, tenderness, distension.
 Limbs: Swelling, pulse quality, temperature to touch.
 Ongoing assessment:
» Continually reassess the patient to determine the effectiveness of emergency interventions
and identify any other injuries or conditions.
» Complete relevant clinical examination (as required)
» EtCO2 (Nasal cannula/ LT – AP and CCP, ETI – CCP)
» Ongoing communication with the family
» Reassess patient condition and vital signs based on interventions given
INITIAL MANAGEMENT
 In patients responding to pain or are unresponsive, open airway or turn lateral, clear (consider
suction) and maintain airway (options include: lateral position or LT in cardiac arrest)
 Provide oxygen as per CPG 3.3 if indicated.
 Rest and reassure patient position of comfort/ appropriate for patient condition, where possible
try to have the parents hold the child to provide comfort.
The situation report to NCC should include the following:

 Exact location (note any dangers encountered)
 Patient age, gender (also include patient status i.e. VVIP etc)
 Provisional Diagnosis or Chief Complaint (e.g. Cardiac chest pain, severe respiratory distress
etc).
 If any CCP / Delta / other services (Police, Civil Defense) support is required
Based on patient severity and time critical nature of

their condition, consider early transport and/or rendezvous
with CCP on route, undertake ongoing assessment
and treatment enroute.
ONGOING ASSESSMENT
 Complete detailed history (full AMPLE history)
 Complete relevant clinical examination (as required)
 EtCO2 (Nasal cannula/ LT – AP and CCP, ETI – CCP)
 Ongoing communication with the family
 Reassess patient condition and vital signs based on interventions given
ONGOING MANAGEMENT
 Consider establishing IV/IO line for drug access or fluid therapy if required – choose an appro-
priate size of cannula for purpose of IV line: smaller cannula for drug access (22g or 20g) and
large bore for fluid administration (18g). NB: Ambulance Paramedics may only establish an IV
on patients under the age of 1 year under direct CCP supervision.
 Specific Management (as per specific Clinical Practice Guidelines)
 Use the following as a guide for specific management requirements:
ENDOTRACHEAL TUBE SIZES:
Age Endotracheal Tube Size
Pre-term 2.5 – 3.0
Term 3.0 – 3.5
1 – 2 Years 4.0 – 4.5
2 – 10 Years (Cuffed) (age/4) + 3.5
2 – 10 Years (Uncuffed) (age/4) + 4
ENDOTRACHEAL TUBE DEPTH:

Depth of insertion: Tube (internal diameter) mm x 3
Depth of insertion (oral) > 2 years: (age/2) + 12 (cm)
Depth of insertion (nasal) > 2 years: (Age/2) + 15 (cm)
FLUID BOLUS:
Neonates: 10ml/ kg
Infants and children: 10 – 20ml/ kg
Maximum: 60ml/ kg
TRANSPORT CONSIDERATIONS
1. Ensure scene time is appropriate for patient presentation – aim for less than 15 minutes in time
critical patients.
2. Initiate transport after immediate life saving interventions in time critical patients and meet with the
CCP en route as per SOP 4.8h
3. Transport to an appropriate facility with pre-notification if required (as per each CPG and pathway)
4. Consider time to hospital vs time to rendezvous with CCP (Do not unnecessarily delay transport)
5. If the patient’s family refuses transport or further care follow SOP 4.8d for on scene discharge.
6. Record final assessment at hospital and ensure patient is handed over to the appropriate staff –
using (SOP 4.8b)
The clinical approach is to be applied to all patients

as a minimum level of care. The only exception is the patient
with an immediate life threatening condition,
as identified by the primary survey, which requires
immediate intervention (eg. CPT ETC)
CPG 13.1 RESUSCITATION OF THE NEWBORN
Assessment Reminders Also Consider
 Is the baby full term?  Narcotic analgesics given?

 Is the baby crying?  Meconium staining?
 Is the baby moving?  Hypoglycaemia
 What is the APGAR at 1 minute?  Hypovolaemia
Dry, warm, position, suction*, stimulate (0-30 seconds)

If spontaneous and effective breathing does not start after 30 seconds:
Provide 5 insufflation breaths

With sustained pressure for 2-3 seconds using room air. If breathing remains inade-
quate or heart rate (on ECG) remains below 100 beats per minute after 30 seconds:
Assisted ventilation with BVM

Continue ventilation at a rate of 40 to 60 breaths per minute. If heart rate (on ECG)
remains below 60 despite good ventilation:
Chest compressions 3:1 ratio

3:1 compression to ventliation ratio. 2 thumbs encircling chest technique on lower
3rd of sternum. Assure ventilation is effective before starting compressions.
LTA
Recommended when chest compressions are initiated or if BVM ventilation is not
effective. If heart rate remains below 60 beats per minute:
Drugs
Adrenaline/ Epinephrine 0.01mg/ kg 1:10 000 IV/ IO every 4 minutes
 *If meconium staining present suction mouth and nose – preferably

with a bulb syringe.
 Assess RBS if baby remains poorly responsive – prick lateral aspect
of the heel.
AP & CCP CCP
CPG 13.1
MANAGEMENT OF NEWBORN AND

NEWBORN RESUSCITATION
MANAGEMENT AIM
To ensure an adequate airway, oxygenation and maintenance of body temperature by drying and pro-
viding a neutral thermal environment. The clinical indicators which suggest the aim is being achieved
are the following:
1. Basic care of the healthy newborn and facilitation of mother to newborn care
2. Recognition of a newborn requiring resuscitative efforts
3. Escalation of care of the newborn with poor ventilation or slow pulse
4. Application of appropriate advanced cardiac life support techniques for newborn resuscitation.
5. Transportation to an appropriate facility with pre-notification and appropriate post-resuscitation
care.
1. Resuscitation is most likely in newborns which are premature (< 37 weeks gestation), difficult de-
livery or antenatal complications. A newborn requiring resuscitation is associated with the following
clinical signs and symptoms:
 Pre-term gestation delivery
 Poor ventilator efforts or weak/ absent cry
 Poor or absent muscle tone (floppy baby)
 Bradycardia or cardiac arrest
 Low SpO2
1. If delivery is imminent, prepare for the delivery and possibility for a neonatal resuscitation. Obtain a
medical and obstetric history from the expecting mother.
2. Ask the following three questions:
 Is the baby term (gestational age ≥ 37 weeks)?
 Is the baby crying and breathing?
 Does the baby have good tone?
3. If the answer to all three questions are ‘Yes’ the baby would generally not require resuscitation
effort and routine care can be provided.
4. After delivery of the baby:
 Position baby in a neutral position (padding behind shoulders) to open the airway
 Stimulate and thoroughly dry with a clean absorbent cloth while assessing breathing, heart
rate, colour and tone.
 Drying is usually sufficient stimulation to induce effective breathing. If spontaneous and effec-
tive breathing is not induced after a brief period of stimulation, further support is indicated (refer
steps of neonatal resuscitation).
 Suctioning should not be performed routinely:
» After birth suctioning with a bulb syringe should only be considered if the airway is ob-
structed or positive pressure ventilation is required.
» Meconium present:
 Vigorous baby with good breathing effort and strong muscle tone – no routine suction-
ing, only consider gentle suctioning from the nose and mouth with bulb syringe to clear
meconium, if necessary.
 In newborn with inadequate breathing effort and poor muscle tone, routine tracheal
suctioning via intubation is no longer recommended and should only be performed in
the event that an obstructed tracheal is suspected. Complete the initial steps of resus-
citation and initiate positive pressure ventilation, if no breathing and heart rate less than
100.
 A bulb syringe is the preferred method of suctioning
 Remove the wet cloth and warm the baby. If the newborn displays good breathing or crying
efforts, good muscle tone and is full term it doesn’t require resuscitation and should be given
to the mother for skin to skin temperature control (and emotional bonding) after drying. Alterna-
tively wrap the baby in the baby blanket to prevent heat loss.
5. Steps of Neonatal Resuscitation:
 After the initial steps at birth, if the baby is gasping or apneic - open the airway and provide 5
insufflation breaths to aerate the lungs. Provide sustained pressure for 2-3 seconds. In term
infants, use room air and either air or low concentration oxygen for preterm newborns. Increase
oxygen to achieve a SpO2 of 85-90% within 10 minutes of birth. Use the lowest oxygen flow
rate to achieve the desired saturation level.
 Re-assess: An increase in heart rate and good chest movement indicates the lungs were
successfully aerated (continue with steps of routine care and give supplemental oxygen if
labored breathing or persistent cyanosis); alternatively continue with the steps of resuscitation,
as appropriate. The above mentioned steps should be completed within 60 seconds. The ECG
should be used to accurately and rapidly estimate the heart rate and a pulse oximeter to moni-
tor oxygenation.
 Most newborns will respond with an increased heart rate within 30 seconds of lung inflation and
aeration. If breathing is inadequate despite an increase in the heart rate or heart rate remains
below 100 beats per minute, continue ventilation at a rate of 40 to 60 breaths per minute and
re-assess to ensure airway is adequately controlled (clear and positioning) with good chest
movement.
 Start chest compressions if the heart rate below 60 despite adequate ventilation and oxygen-
ation.
» Check heart rate every 30 seconds and discontinue chest compressions if heart rate above
60 beats per minute.
» Use 100% oxygen whenever chest compressions are performed and wean oxygen con-
centration when heart rate recovers.
» Use a compression-ventilation ratio of 3:1 at a rate of 120 events per minute (90 compres-
sions : 30 ventilations). Compress the chest 1/3 of the depth either by encircling the chest
with both hands and compressing with the thumbs (two thumb technique) or using 2 fingers
of one hand while supporting the back with the other. Allow the chest to recoil completely
after each compression. The two thumb technique is preferred as it causes less rescuer
fatigue while generating a higher blood pressure and coronary perfusion pressure.
 Medication:
» Drugs are rarely indicated in neonatal resuscitation. Establishing adequate ventilation is
the most important step in correcting bradycardia. However, if the heart rate remains below
60bpm despite adequate ventilation, consider adrenaline and/ or volume expansion.
» A route for drug administration is required as the endotracheal route may be ineffective. IV
and IO have been shown to be effective routes for drug administration thus the choice as
to which should be used is up to the practitioner in the clinical situation.
» Adrenaline/ Epinephrine is given every 4 minutes during resuscitation (0.01mg/ kg.
1:10 000)
» Consider hypovolemia as cause of cardiac arrest – fluid bolus of 10ml/ kg.
6. Routine care for healthy baby:
 Assess the APGAR score at 1 minute but the APGAR score should not be used to determine
the need for neonatal resuscitation
 Delay cord clamping:
» Delayed clamping is defined as cord clamping between 30 seconds to three minutes after
birth.
» Do not clamp or cut the cord, unless the infant requires earlier intervention (positive pres-
sure ventilation), the recommendation is to wait for 60 seconds then clamp the cord. Keep
the newborn below the level of the placenta to allow gravity to assist in transfusing blood
through the cord.
» Place the first clamp approximately 10-15cm from the newborn’s umbilicus. Then place
a second clamp after the segment between the 2 clamps has been milked. The cord can
then be cut in a relatively bloodless manner.
 Prevent and treat Hypoxia, Hypothermia and Hypoglycemia:
» Maintain the newborn’s temperature between 36.5 – 37.5ºC. Maintaining body tempera-
ture within the range is important as it is strongly associated with mortality and morbidity as
well as to prevent hypoglycaemia and hypoxia. Skin to skin care is advocated as the best
process for creating a neutral thermal environment and to stimulate bonding between the
newborn and the mother.
» The newborn baby’s blood sugar should be assessed (prick the lateral aspect of the heel).
It is particularly important to assess the blood glucose of babies born prematurely or from
mothers with diabetes. If the blood glucose is less than 2.6mmol/l and the baby is alert
with a good suction reflex, initiate breast feeding or administer oral glucose. If baby floppy
with poor ventilation effort administer IV Dextrose 10% at 2ml/kg, if blood sugar less than
2.6mmol/l.
» Consider supplemental oxygen at a flow rate of 2 - 6L/ min (28 to 40%) to maintain a target
SpO2 of between 90% and 95%, for any newborn presenting with signs and symptoms of
respiratory distress (nasal flaring, recession, tachypnea) after delivery. Supplemental oxy-
gen should not be routinely administered.
 The APGAR score should be repeated after 5 minutes.
 The World Health Organization (WHO) recommends that breastfeeding is initiated within the
first hour of birth. The newborn should be placed skin to skin following birth for at least an hour
and the mother should be encouraged to initiate breast feeding when the newborn is ready to
do so.
 Continue to monitor the following en route to hospital:
» Heart Rate
» Respiratory Rate
» SpO2
» Temperature
» RBS (only repeat if initially low)
 If resuscitation is required transport all newborns to appropriate facility with CPR, priority 1.
Alternatively transport priority 2. Pre-notify the receiving facility in order to prepare to receive
the newborn.
CPG 13.2
MANAGEMENT OF PAEDIATRIC
CARDIAC ARREST
MANAGEMENT AIM
To recognise patients for whom resuscitation is indicated, immediately initiate intervention to restore
perfusion to the brain and other organs and transport to appropriate facility for further interventions or
after return of spontaneous circulation. The clinical indicators which suggest the aim is being achieved
are the following:
the latest international guidelines on resuscitation.
4. Advanced Cardiac Life Support and post cardiac arrest therapy to prevent reoccurrence of cardiac
arrest.
In paediatrics, cardiac arrest is most commonly secondary to hypoxia (choking, near drowning and
respiratory diseases).
Assess the patient for cardiac arrest by looking for movement or normal breathing. If these are absent
then a pulse check (brachial in < 2 years old) may be undertaken, which may be difficult to feel. Pal-
pate the brachial/ carotid pulse for no MORE than 10 seconds. If no pulse is found or you are uncer-
tain then first initiate chest compressions while preparing ventilation equipment.
Patients not viable for resuscitation are those with irreversible brain death:
 Decapitation or brain protruding
 Dependent lividity or rigor mortis
 Decomposition
PAEDIATRIC CARDIAC ARREST

(See Algorithm below)
1. Initial approach as per CPG 13: Clinical approach to the paediatric patient.
2. Provide 5 effective ventilations via BVM.
3. Start chest compressions, use a compression/ ventilation ratio of 30:2 for 1 rescuer or 15:2 for
two rescuers, at a rate of 100 to 120 compressions per minute with a compression depth of 4cm
in infants and 5 cm in children; allow the chest to recoil completely after each compression. Take
approximately the same amount of time for each compression and relaxation. Remember to PUSH
HARD and PUSH FAST. Minimize the interruption in chest compressions. Change person provid-
ing the compressions every 2 minutes to ensure maximum effectiveness of compressions due to
fatigue.
4. While the first 30 chest compressions are being given the second crew person can open the
airway by placing a pad beneath the shoulders (or head-tilt). Provide two ventilations with a bag-
valve-mask, using an inspiratory time of one second until chest begins to rise, avoid over-inflation
as this reduces venous return. Do not delay chest compressions to insert an airway, which should
be inserted during compressions.
 If BVM fails to provide adequate ventilation then undertake supraglottic airway intubation. Inter-
ruption of chest compressions for LTA insertion should be no more than 10 seconds. If an LTA
is inserted its placement should be confirmed using continuous quantitative EtCO2 waveform
as well as visualisation and auscultation.
5. During resuscitation provide ventilation with supplemental oxygenation at a ratio of 2 ventilations
to 30 compressions (single rescuer) or 2:15 (for 2 or more rescuers). If LTA is performed provide
ventilation at a rate of 8-10 breaths per minute with continuous chest compressions.
6. Place the defibrillation pads on the patient’s bare chest while chest compressions are in progress,
use adult pads in the anterior-posterior position on the chest. Analyze the rhythm:
 If the rhythm is shockable: Ventricular Fibrillation or Ventricular Tachycardia – Change the
defibrillator with an energy setting of 4J/kg while continuing chest compressions. The person
performing the compressions then stops, “clears” for defibrillation and defibrillates the patient
and immediately begins compressions again. A cycle of 2 minutes of CPR is continued before
another rhythm check. Minimise interruption to chest compressions to check the rhythm.
 If the rhythm is non-shockable: Asystole or Pulseless Electrical Activity – continue with a cycle
of 2 minutes of CPR before another rhythm check. Minimise interruption to chest compressions
to check the rhythm.
7. Drug administration has not been shown to improve survival although it has demonstrated im-
proved rates of ROSC. A route for drug administration is required as the endotracheal route may
be ineffective or potentially cause a worse outcome (adrenaline/ epinephrine) and certain drugs
have not been shown to be safe via the ETT route (Amiodarone). IV and IO have been shown to
be effective routes for drug administration thus the choice as to which should be used is up to the
practitioner in the clinical situation. Adrenaline/ Epinephrine is given every 4 minutes during resus-
citation. The first dose is given after the first unsuccessful shock is delivered. Amiodarone is given
when VF or VT is deemed refractory to defibrillation (after the 3rd, 4th and 5th shock). Maximum
single dose of Amiodarone is 300mg. If patient is >60kgs. use adult dose. Magnesium can be giv-
en when Torsades de Pointes is present.
8. If hypoglycemia is confirmed, administer 2.5ml/ kg D10 in maximum increments of 50ml. Re-check
RBS and repeat dose if RBS remains <4mmoL.
9. Parameters indicating ROSC include central pulses, rise in EtCO2 and pulse oxymetry. A palpa-
ble central pulse when compressions are interrupted is a reliable indicator of ROSC. The abrupt
and persistent rise in EtCO2 to normal values (35-45 mmHg) is a good indicator of ROSC. Pulse
oxymetry is a poor indicator of quality during resuscitation but may indicate ROSC when strong
waveform returns.
10. Termination of paediatric resuscitation should not occur in the field – transport to an appropriate
facility with CPR in progress.
POST-RESUSCITATION CARE
1. Optimize oxygenation and ventilation to maintain a SpO2 ≥95%. Assist ventilation if significant re-
spiratory compromise. If intubated or LTA – ensure patency – verify tube position and continuously
monitor EtCO2. Insert gastric tube.
2. If an advanced airway is in place (LTA, ETT) the CCP may consider sedation and paralysis in
order to maintain the airway and effective ventilation. If no CCP is available the AP should remove
the LTA if the patient begins to gag or ‘fight’ the LTA and use appropriate airway maneuvers to
maintain SpO2 ≥ 95%.
3. Ventilation – in intubated patients ventilation should be maintained with a mechanical ventilator.
Include ventilator settings per age: Rate: age dependent, TV 6 – 8 ml/kg, FiO2: maintain SpO2 of
≥ 95%, Pmax: 18 – 25cmH2O (age dependent), PEEP: 3-5 cmH2O, I:E ratio: 1:1 (neonates), 1:2 –
age dependent
4. Maintain mean arterial pressure of greater than 65mmHg using fluid boluses or inotropes:
 Consider 10 to 20ml/ kg fluids bolus if signs and symptoms of shock – consider underlying
cause
 Consider inotropic infusion if shock persist: Adrenaline/ Epinephrine
5. Monitor and treat any seizures (Midazolam) and hypoglycaemia. Avoid hyperglycaemia.
6. Sedation and paralysis of the patient after ROSC should not be used routinely except when there
is a risk of self-injury or when the patient is being ventilated to facilitate improved ventilator com-
pliance. Consider analgesia (Fentanyl), sedation (Midazolam or Ketamine) and neuromuscular
blocking (Rocuronium) if dyssynchrony between patient and ventilator or severely compromised
ventilation function.
PAEDIATRIC DEFIBRILLATION ENERGY SETTING
Weight VF/pVT (4 J/kg) Synchronized Cardioversion

1 J/kg 2 J/kg
3 kg 10 Joules 3 Joules 6 Joules
6 kg 30 Joules 6 Joules
8 kg 8 Joules
12 kg
16 kg 70 Joules
18 kg 20 Joules
28 kg
31 kg 125 Joules
34 kg 70 Joules
37 kg 150 Joules
40 kg
CPG 13.3.1
MANAGEMENT OF ACUTE FOREIGN

BODY AIRWAY OBSTRUCTION IN
PAEDIATRICS
MANAGEMENT AIM
To identify the site and cause of the partial or complete foreign body airway obstruction and to apply
an appropriate treatment intervention, to improve ventilation and oxygenation. The clinical indicators
which suggest the aim is being achieved are the following:
1. Identify the occurrence of an acute partial or complete foreign body airway obstruction.
2. Relieve or limit the airway obstruction utilizing appropriate interventions.
3. Improved SpO2 levels (≥ 95%).
4. Transport patient promptly without delay and pre-notify the receiving facility.
1. Signs and symptoms indicative of a foreign body airway obstruction:

 Sudden onset of respiratory distress or arrest possibly with coughing, gagging, stridor or
wheezing. There is no recent history of upper respiratory tract infection. Possibly a history of
eating or playing with objects prior to the onset of signs and symptoms.
Stridor Definition: An abnormal high-pitched sound caused by turbulent airflow through a par-
tially obstructed upper airway (supraglottis, glottis, subglottis and trachea)
CAUSES OF ACUTE STRIDOR:
 Croup, FBAO, Epiglottitis, Anaphylaxis
 Bacterial Tracheitis, Retropharyngeal or peritonsillor abscess
Initial approach as per CPG 13: Clinical approach to the paediatric patient, obtaining an appropriate
history especially the timing of onset and events leading to.
FBAO PARTIAL OBSTRUCTION – COUGHING EFFECTIVELY

Signs of effective coughing:
 Fully responsive
 Loud and forcefully coughing
 Able to breath between coughs
 Verbally responsive or crying
1. Encourage forcefully coughing and administer oxygen via face mask.
2. Monitor continuously for progression to a complete FBAO.
3. Transport promptly and without delay (Priority 2 – to keep child calm) with pre-notification of the
receiving facility.
FBAO COMPLETE OBSTRUCTION – COUGHING INEFFECTIVELY

Signs of effective coughing:
 Unable to vocalize
 Unable to breath
 Silent cough
 Cyanosis
 Decreasing level of consciousness
CONSCIOUS INFANT/ CHILD:

 Infant: Give repeated 5 backslaps (hold infant head down) followed by 5 chest thrusts until the
object is expelled or the infant becomes unconscious.
 Remember: Abdominal thrusts are not recommended for infants – high risk of injuring to the
liver.
 Child: Give repeated sub-diaphragmatic abdominal thrust or backslaps until the object is ex-
pelled or the child becomes unconscious.
UNCONSCIOUS INFANT/ CHILD:
 Initiate chest compression, if patient became unconscious (no pulse check).
 After 30 compressions open the airway and remove FBAO if visible – no blind finger
sweep.
 Attempt 2 ventilations – Open the airway - head tilt chin lift and assess the
effectiveness of ventilation attempts (chest rise and fall).
 Continue with cycles of chest compressions and ventilation (30:2 one rescuer and
15:2 for two rescuers) until FBAO removed.
 CCP: use an appropriately sized laryngoscope and pediatric magill’s forceps to
visualize and remove the obstruction.
 If the obstruction cannot be removed use a needle cricothyroidotomy to ventilate the
child while transporting to hospital priority 1 with pre-notification.
Transport priority: The decision to transport must be made early and without delay. Ensure quick
 If the child cannot be ventilated by needle cricothyroidotomy attempt to push the
and safe transportation to the closest and most appropriate medical facility with pre-notification.
obstruction further down the trachea into one of the bronchi and then ventilate one
lung. This is risky and should only be done in extreme situations.
CPG 13.3.2MANAGEMENT
CPG 13.3.2 MANAGEMENT OF CROUP OFAND EPIGLOTTITIS
CROUP AND EPIGLOTTITIS
Assessment Reminders: Other Conditions to consider:

 Recent URTI?  FBAO
 Rapid onset  Anaphylaxis
 Croup age group = 3 months – 3 years  Laryngeal trauma
 Epiglottitis age group = 2 – 6 years  Inhalation injury
 Fever? Cough? Hoarse voice?
Management of Epiglottitis:
 Keep the child calm and allow the parent to hold the child in a position of comfort.
 Transport sitting up.
 Administer oxygen if tolerated by the child.
Management of Croup:
 Identify level of severity of croup
o Mild Croup: Modified Westley Score ≤ 2
o Moderate Croup: Modified Westley Score: 3 – 7
o Severe Croup: Modified Westley Score: ≥ 8
Mild Croup Moderate Croup Severe Croup

 Dexamethasone:  Dexamethasone:  Dexamethasone:
0.6mg/kg orally OR 0.6mg/kg orally OR 0.6mg/kg orally OR
 Budesonide 2mg  Budesonide 2mg  Budesonide 2mg
Nebuliser Nebuliser Nebuliser

 Adrenaline Neb:
If patient has any stridor at 0.5mg/kg (Max 5mg)
rest, decreased air entry,
intercostal recession or  If airway obstructs:
changes in LOC or cyanosis Cricothyrotomy
(Quicktrach II)
Consider: 
 Adrenaline Neb:
0.5mg/kg (Max 5mg)
NOTE:
 Do not upset the child as this will increase levels of distress. In Epiglottitis this could obstruct the airway.
 Allow the parent to hold the child and comfort the child.
 Do not drive P1 unless the airway becomes compromised.
AP & CCP CCP
CPG 13.3.2
MANAGEMENT OF CROUP AND

EPIGLOTTITIS
MANAGEMENT AIM
To identify the site and cause of the partial or complete airway obstruction and apply an appropriate
intervention to improve ventilation and oxygenation. The clinical indicators which suggest the aim is
1. To relieve or limit the airway obstruction utilizing appropriate interventions.
2. Improved SpO2 levels (≥95%)
3. Limit the risk of complete obstruction occurring in infective lower airway inflammation.
Infective diseases which can produce airway obstruction include epiglottitis and croup. These condi-
tions produce inflammation which either creates a mechanical obstruction (epiglottitis) or a significant
narrowing of the airway (croup). Croup occurs most frequently in children 6 months – 3 years old and
epiglottitis in the 2-6 year old age group. Assess the history, especially the timing of onset and if the
child had a sore throat or fever over the past few days. Tracheal intubation is rarely required.
1. Epiglottitis: The child presents with high fever following a sore throat. The child assumes a tripod
position, looks ‘toxic’, is extremely anxious and may be drooling as swallowing is extremely difficult
and they have a muffled voice if able to speak. Onset and progression of symptoms for epiglottitis
is over hours rather than days (short onset).
2. Croup: The condition starts with upper respiratory infection and spreads down producing a
barking cough, stridor and a hoarse voice. The child will look ‘well’ and can often lie supine
despite displaying signs of respiratory distress. Croup is considered severe when associated
with use of accessory muscles (sternal retraction and paradoxical chest movements) and
changes in level of consciousness. Onset and progression of symptoms for croup is over days
rather than hours (slow onset). Use the Westley clinical scoring system for croup to assess
severity.
COMPARISON OF CLINICAL FEATURES OF CROUP AND EPIGLOTTITIS:
Croup Epiglottitis
Aetiology Parainfluenza virus Haemophilus Influenza Type B
Age of patient 6 months – 3 years 2 – 7 years
Onset of disease Gradual Sudden
Fever Mild >38ºC
Swallowing Normal Difficult with drooling
Coughing Barking cough Supressed
Voice Hoarse Muffled
General appearance Well Toxic
MODIFIED WESTLEY CLINICAL SCORING SYSTEM FOR CROUP (for <6 years old)
0 points 1 point 2 points 3 points 4 points 5 points
Inspiratory None When aggitated At rest

stridor
Intercostal None Mild Moderate Severe

recession
Air Entry Normal Mildly de- Severely

creased decreased
Cyanosis None With At rest

Agitation /
activity
LOC Awake Altered
Total Possible Score 0-17:

≤2=mild croup, 3-7=moderate croup, ≥8=severe croup
1. Initial approach as per CPG 13: Clinical approach to the paediatric patient
2. Management of mild, moderate and severe croup: Dexamethasone 0.6mg/kg orally if child can swallow
(max 10mg) OR Budesonide 2mg Nebuliser if child unable to take oral dexamethasone.
3. In moderate to severe croup nebulise the child with Adrenaline/ Epinephrine 0.5mg/kg (max 5mg)
if indicated if. This helps reduce the swelling. ECG monitoring is required during the procedure to
avoid side effects. Transport the child in position of comfort and without upsetting the child,
priority 2 to hospital.
4. In Epiglottitis provide supplemental oxygen, transport the child in the tripod position, priority 2 and
notify the hospital of the situation.
If the child develops complete airway obstruction undertake

a needle cricothyrotomy and use BVM ventilation to
maintain oxygenation. In this circumstance it is reasonable
to transport the child Priority 1.
5. Create a calm environment and limit the number of people present. Avoid upsetting the distressed
child with stridor as crying and agitation increase respiratory effort and might precipitate complete
airway obstruction. The child should be allowed to adopt the posture in which they are most com-
fortable. The parent should continue to handle the child. Keep your distance. Examination of the
throat and IV cannulation should not be attempted.
Gentle examination such as touching to assess temperature

or application of pulse oxymetry may be tolerated but
should be aborted immediately if the child is not cooperating
as any finding will not change the decision to transport child
to hospital with pre-alert.
CPG 13.4 MANAGEMENT OF ANAPHYLAXIS IN PAEDIATRICS
 Sudden onset?  Idiopathic angio-oedema

 Likely Cause?  Asthma
 CVS, Respiratory, GIT symptoms?  Seizures
 Airway involvement?  Anxiety attacks
 Skin signs alone NOT anaphylaxis
First line medications:

 Adrenaline/ Epinephrine 0.01mg/kg IM (max 0.5mg) – repeat
after 5 minutes if required
 < 6yrs: 0.15mg (0.15ml)
 6 -12 yrs: 0.3mg (0.3ml)
 > 12 yrs: 0.5mg (0.5ml)
 IV fluids: 10-20ml/ kg (repeat to max 60ml/kg)
Second line medications:
 Salbutamol Neb 5mg
 Upper airway swelling? Adrenaline/ Epinephrine Neb 0.5mg/ kg
(max 5mg)
 Complete airway obstruction: cricothyrotomy

 Ipratropium Bromide Neb 0.25 - 0.5mg
 Diphenhydramine IV/ IO/ IM 1mg/ kg (max 50mg) dilute for IV/ IO
 Hydrocortisone IV/IO 5mg/kg (max 200mg)
 Adrenaline/ Epinephrine 0.05 - 0.3 mcg/ kg/ min
 Dilute 2mg of 1:1000 with 18ml NS in 20cc syringe
 Administer using syringe driver at 0.05 to 0.3mcg/ kg/ min
Priority 1 transport if airway compromised or CV collapse

unresponsive to therapy
AP & CCP CCP
CPG 13.4
MANAGEMENT OF ANAPHYLAXIS IN
PAEDIATRICS
MANAGEMENT AIM
The management aim is to identify anaphylaxis early and initiate interventions to relieve signs and
symptoms and prevent life threatening complications. The clinical indicators which suggest the aim is
1. Early recognition of impending airway compromise.
2. Relief of upper airway obstruction and/or bronchoconstriction to keep SpO2 levels ≥ 95%.
3. Hemodynamic status returning to normal levels.
4. Prevention of delayed onset cardiovascular collapse.
Anaphylaxis is associated with one or all of the following clinical symptoms:

1. Angio-oedema of the airway with hoarse voice, stridor, and obvious swelling of the face and neck.
2. Wheezes, tachypnoea, and used of accessory muscles.
3. Hypotension, tachycardia, and cardiovascular collapse with cardiac arrhythmias.
4. Skin reactions including rash, hives, itching and swelling (skin reactions alone are not considered
anaphylaxis.
1. Initial assessment: As per CPG 13: Clinical approach to the paediatric patient, obtaining an appro-
priate history especially the timing of onset and allergies, conduct a physical assessment (airway,
respiratory, cardiovascular and skin involvement) and base line vital signs (pulse rate, respiratory
rate, SpO2, BP, Capillary refill, GCS, RBS and temperature).
2. Initiate supplemental oxygen therapy (CPG 3.3) via NRB mask or nasal cannula aiming to achieve
a SpO2 ≥ 95%
3. First line medication:
 IM Adrenaline/ Epinephrine is recommended as the first line medication in the management of
anaphylaxis. Adrenaline/ Epinephrine should be immediately administered in the anterolateral
aspect of the middle third of the thigh of any patient with signs and symptoms of anaphylaxis.
4. Second line medications:
 Signs of upper airway oedema (stridor, hoarse voice, angioedema):
» Nebulize with Adrenaline/ Epinephrine
» Complete airway obstruction: Undertake a needle cricothyrotomy and use BVM ventilation
to maintain oxygenation. In this circumstance it is reasonable to transport the child Priority
1.
 Signs of bronchoconstriction (wheezing) treat according to CPG 13.5 (paediatric bronchocon-
striction)
 Establish IV or (IO if IV not available) – large bore cannula: Consider administering a fluid chal-
lenge of 10-20 ml/kg, if presenting with signs and symptoms of shock (tachypnoea, tachycar-
dia, weak peripheral pulses, delayed capillary refill, mottled skin colour, altered LOC), reassess
and repeat as necessary to a max of 60 ml/kg.
 Consider administering Diphenhydramine
 Consider administering Hydrocortisone IV
 In extremis Adrenaline/ Epinephrine infusion. This is potentially hazardous but can be life sav-
ing.
CPG 13.5 PAEDIATRIC ACUTE BRONCHOCONSTRICTION MANAGEMENT
 Is patient using bronchodilators  Pneumonia

 Is there a persistent dry cough with  Bronchiolitis
wheezing on auscultation  Croup/ Bronchitis
 Respiratory Rate?  Aspiration syndrome
 Use of accessory muscles, tracheal
tugging, abdominal breathing
 Salbutamol 2.5 - 5mg nebulized

 Agitated and un-
 Ipratropium Bromide 0.25-5mg nebulized
able to vocalise
S  Confusion
E  Low SpO  Adrenaline/ Epinephrine 0.01mg/kg IM max
2
V 0.3mg for life threatening asthma
 HR >140 (2-5yrs)
E
or >125 (>5yrs)  Hydrocortisone 5mg/kg max 200mg IV
R  Magnesium 25-50mg/kg IV (if not responding
E  RR >40 (2-5yrs) to other therapy) max 2g over 20 minutes
or >30 (>5yrs)
 IV Salbutamol 10mcg/kg (max 250mcg) if no
 Silent Chest response to nebulization
M  Salbutamol 2.5 - 5mg nebulized

O  Wheezing or dry
D cough  Ipratropium Bromide 0.25 - 5mg nebulized
E  Alert but agitated
R
A  HR 120-140
 Hydrocortisone 5mg/kg IV max 200mg
T  RR >30
E
 Wheeze or dry
M cough
I  Talks/ vocalise
normally  Salbutamol 2.5 - 5mg nebulized
L
D  RR < 30  Ipratropium Bromide 0.25 - 5mg nebulized
 Alert
 If patient has life threatening condition, initiate priority 1 transport

and if possible meet CCP en route WHILE undertaking treatment
AP & CCP CCP
CPG 13.5
TIME CRITICAL INTERVENTION LIFE THREATENING
BRONCHOCONSTRICTION
MANAGEMENT AIM
To relieve bronchoconstriction, decrease the work of breathing and improve ventilation and oxygen-
ation. The clinical indicators which suggest the aim is being achieved are the following:
1. Improved SpO2 levels (≥ 95 %)
2. Vital signs returning to normal levels
3. Cessation of wheezing and return of normal air sounds on auscultation
4. Improved patient breathing comfort (a very subjective and inaccurate indicator)
Bronchoconstriction is associated with the following clinical signs and symptoms:

1. Bilateral wheezing over all lung fields, associated with dry coughing and patient complaining of a
tight chest. Wheezes might be less apparent with increasing airway obstruction. A silent chest is
an ominous sign in an acutely breathless patient indicating very little ventilation is happening.
2. Use of accessory muscles as noted by head bobbing, tracheal tugging, and abdominal breathing.
3. Nasal flaring, intercostal and subcostal recession (or retraction) is indicative of an increase in work
of breathing.
4. Pulse rate: An increasing pulse rate generally indicate worsening bronchoconstriction, a decrease
in the pulse can represent improvement or be a sign of impending cardiac failure. Bradycardia is a
pre-terminal event in life-threatening bronchoconstriction.
LEVEL OF SEVERITY IN PAEDIATRIC ACUTE ASTHMA
Moderate Asthma Severe Asthma Life-threatening Asthma
Alert but may be agitated Agitated Confusion
Unable to talk sentences Too breathless to talk Exhaustion
Decreased activity and feeding Decreased activity, stop feeding Unable to feed
SpO2 ≥ 92% SpO2 < 92% SpO2 < 92%
Heart Rate: Heart Rate: Cyanosis
2-5 Years: ≤ 140 beats per min 2-5 Years: > 140 beats per min Poor respiratory effort
> 5 Years: ≤ 125 beats per min > 5 Years: > 125 beats per min Hypotension
Respiratory Rate: Respiratory Rate: Silent chest
2-5 Years: ≤ 40 breaths per min 2-5 Years: > 40 breaths per min
> 5 Years: ≤ 30 breaths per min > 5 Years: > 30 breaths per min
Obtain an appropriate history especially previous episodes of breathlessness, cough, chest infections
and family history of allergy, conducting a physical assessment (breath sounds, use of accessory
muscles and symmetry of movement) and base line vital signs (Pulse rate, respiratory rate, SpO2, BP,
capillary refill, GCS, RBS and temperature)
2. Administer Salbutamol nebulized, repeat if necessary.
3. Consider adding Ipratropium Bromide nebulization to initial Salbutamol in cases of moderate to
severe bronchoconstriction.
4. Consider administering Hydrocortisone IV in moderate to severe bronchoconstriction.
5. In paediatrics who have not responded to the therapy outlined above, consider Second line treat-
ment in children 2 years and older:
 Consider administering IV Magnesium to patients with acute severe bronchoconstriction unre-
sponsive to therapy or patients with near fatal bronchoconstriction.
 Consider administering IV Salbutamol in severe and/ or life-threatening bronchoconstriction with
minimal or poor response to initial therapy.
6. Depending on the situation IV access may be difficult or the patient may be met in extremis Adren-
aline/ Epinephrine IM may also be an initial option in very severe exacerbations of asthma and in
situations where other treatment options are not available within reasonable time.
CPG 13.6 MANAGEMENT OF PAEDIATRICS SEIZURES
 Is the area around the patient safe?  Hypoxia

 Rule out reversible causes  Hypoglycaemia
 Past history of seizure?  Emotional disturbance
 Fever?  Hyperpyrexia
 Provide oxygen if seizures prolonged (> 5 minutes)

 Passive cooling if pyrexia present – remove blankets and clothing,
do not allow shivering as this increases body temperature
 Febrile seizures: Oral Paracetamol if the patient is alert and can
swallow (120mg in 5ml syrup)
 Paediatrics: 15mg/ kg
 Infants: 7.5mg/ kg
 Midazolam:
 IN 0.2mg/ kg (max 1ml/ nostril/ dose)
 IM: 0.2mg/ kg – up to maximum of 10mg per injection, repeat
after 15 minutes if required
 IV/IO: 0.1mg/ kg in increments of 5mg, up to maximum of 10mg,
repeat after 5 minutes if required
 Febrile seizures: Oral Paracetamol if the patient is alert and can
swallow (120mg in 5ml syrup)
 Paediatrics: 15mg/ kg
 Infants: 7.5mg/ kg
 The IN route is preferred if no IV in situ

 Only administer Midazolam for prolonged (> 5 minutes) or recurrent
seizures (status epilepsy)
AP & CCP CCP
CPG 13.6
SEIZURES
MANAGEMENT AIM
To recognize seizures and febrile seizures and initiate cooling and anticonvulsant intervention to pre-
vent end organ damage especially to the brain. The clinical indicators which suggest the aim is being
2. Recognizing seizures and eliminating possible causes.
3. Preventing convulsion related secondary harm.
4. Post convulsion management to prevent further seizures.
1. Tonic phase: sudden onset generalized contraction of all voluntary muscles and loss of conscious-
ness. A moan may be produced by the contractions of the respiratory muscles, which also pre-
vents normal breathing.
2. Clonic phase: Repeated contraction and relaxation of the muscles including respiratory muscles
causing hypoxia.
3. Post-ictal phase: the patient goes through a period of unconsciousness followed by confusion be-
fore regaining full mental capacity. The patient may vomit during this phase and may have exces-
sive salivation. The patient will experience fatigue and headache once fully awake.
4. Witnessing a seizure can be distressing. Steps outlined under point 3 below are usually all that is
required. Reassure staff and relatives around you. Proceed to drug management only if seizures
are prolonged. A prolonged seizure is defined by convention as seizure lasting longer than five
minutes.
5. It is prudent to institute drug management earlier if adequate oxygenation cannot be achieved with
basic airway manoeuvres and high flow oxygen.
1. Initial approach as per CPG 13: Clinical approach to the paediatric patient, obtaining an appro-
priate history (specifically of epilepsy, recent head injury and sudden onset of fever) and number
and timing of the seizures, conducting a physical assessment and base line vital signs (pulse rate,
respiratory rate, SpO2, BP, capillary refill, GCS, RBS and temperature)
2. Exclude hypoxia, hypoglycaemia and fever as a cause of the seizures. If these are present treat
with oxygen or according to the hypoglycaemia (CPG 7) guideline. If febrile, cool the child utilizing
passive cooling measures. If suspected heat stroke, treat according to the heat stroke (CPG 10.1)
guideline.
3. If active seizures or post-ictal phase place in the lateral position and monitor for vomiting. Suction
the airway as required (there may be excessive salivation following seizures)
4. Persistent seizures: In a patient with persistent (> 5 minutes) convulsions administer Midazolam
during the convulsion. Alternative routes to IV of drug administration are recommended as a first
line/ initial treatment in pre-hospital management of paediatric seizures.
 Administer Midazolam IN (preferred)/ IM/ Buccal.
 Repeat once within 5 minutes if seizure persists or reoccurs.
 In the event that an IV therapy is established upon arrival, an IV dose should be administered.
5. If within short distance of an appropriate medical facility, transportation should not be delayed to
establish IV therapy, as alternative routes of drug administration are as effective.
6. If seizures due to pyrexia (febrile convulsions) administer oral Paracetamol.
 Oral Paracetamol (only administer to a fully alert child)
 Remember to utilize passive cooling measures (undress, remove blankets, good air flow) but
do not allow shivering as this will raise body temperature.
CPG 13.7
MANAGEMENT OF SYMPTOMATIC
PAEDIATRIC ARRYTHMIAS
CPG 13.7.1 MANAGEMENT OF PAEDIATRICS SYMPTOMATIC BRADYARRYTHMIAS

 Decreasing LOC  Hypoglycaemia
 Hypotension  Raised ICP
 Signs of shock  Severe hypovolaemia
 Airway management and oxygen therapy

 Pulse < 60 start chest compressions
 DO NOT compromise effective oxygenation or chest compressions
to perform IV cannulation
 If patient deteriorates into cardiac arrest follow CPG 13.2 (page 191)
 No response to chest compressions and adequate ventilation?

 Adrenaline/ Epinephrine: IV/IO 0.01mg/ kg max 0.5mg
 If due to increased vagal tone give Atropine: IV/IO 0.02mg/ kg
(min 0.1mg and max 0.5mg), repeat if required
 Fluid bolus 10-20 ml/kg of NS if hypotensive
 If patient becomes pulseless start cardiac arrest guideline
AP & CCP CCP
CPG 13.7.1
SYMPTOMATIC BRADYARRHYTHMIAS
MANAGEMENT AIM
To recognize bradycardia and initiate appropriate intervention to revise any treatable causes. The clini-
1. Improved SpO2 levels (≥ 95 %)
2. Recognizing bradycardia with signs and symptoms of poor perfusion.
3. Treat reversible causes of bradycardia.
4. Administration of Adrenaline, if bradycardia persists despite adequate ventilation.
5. Transport promptly to the closest most appropriate medical facility.
Aetiology of paediatric bradycardia:

1. Hypoxia
2. Hypothermia
3. Raised intracranial pressure
4. Electrolyte imbalances
5. Acidosis
6. Severe hypovolemia
Obtain an appropriate history (specifically of past medical history, recent illness, history of cardiac
problems), conducting a physical assessment and base line vital signs (AVPU, pulse rate, respiratory
rate, SpO2, BP, capillary refill, GCS, RBS and temperature).
2. In a paediatric with bradycardia and poor perfusion (altered mental status, hypotension and signs
of shock):
 Identify and treat possible reversible causes (hypoxia is the most common cause of bradycar-
dia in paediatrics).
 Open and assess airway (place child in neutral or sniffing position).
 Initiate oxygen (CPG 3.3) therapy with one of two options: Use a non-rebreather mask if res-
piration (rate, depth and volume) adequate or bag-valve-mask (BVM) assisted ventilation, if
respiration inadequate.
 Poor perfusion persists despite adequate oxygenation and ventilation:
» If pulse less than 60 start chest compression.
» After 2 min, if bradycardia persists, administer Adrenaline/ Epinephrine
» If bradycardia secondary to increased vagal tone or AV block, administer Atropine
» Reassess pulse every two minutes, if condition improves with treatment, provide support-
ive care
 Establish IV/IO – consider fluid bolus, if signs and symptoms of hypovolaemia
3. Change to cardiac arrest protocol, if patient become pulseless.
CPG 13.7.2 MANAGEMENT OF PAEDIATRICS SYMPTOMATIC TACHYARRYTHMIAS

 Decreasing LOC  Fever
 Hypotension  Hypoglycaemia
 Signs of shock (cold limbs, mottled  Severe hypovolaemia
skin, delayed capillary refill time)
 Attempt Valsalva (Blow on 10ml syringe –15 seconds duration)
 Narrow Complex Tachyarrhythmia

 Immediately life threatening: Synchronised cardioversion 1J/kg,
increase to 2J/kg
 Symptomatic:
 Adenosine 0.1mg/kg with flush, repeat 0.2mg/kg with flush
 Wide Complex Tachyarrhythmia

 Immediately life threatening: Synchronised cardioversion 1J/kg,
increase to 2J/kg
 Symptomatic:
 Amiodarone 5mg/kg over 20 minutes
 If patient becomes pulseless start cardiac arrest guideline.
AP & CCP CCP
CPG 13.7.2
SYMPTOMATIC TACHARRHYTHMIAS
MANAGEMENT AIM
To recognize tachycardia and initiate appropriate intervention to revise any treatable causes. The clini-
2. Recognizing tachycardia and signs and symptoms of poor perfusion.
3. Interpret ECG to differentiate between sinus tachycardia, supraventricular tachycardia and ventric-
ular tachycardia.
4. Provide appropriate treatment in-line with the ECG rhythm and clinical condition.
5. Transport promptly to the closest most appropriate medical facility.
Obtain an appropriate history (specifically of recent illness, past medical history, medication and previ-
ous episode) and number and timing of the seizures, conducting a physical assessment and base line
vital signs (AVPU, pulse rate, respiratory rate, SpO2, BP, capillary refill, GCS, RBS and temperature)
2. During assessment recognize tachycardia:
 Consider oxygen and fluid bolus, if signs and symptoms of hypoxia and hypovolaemia are
present.
3. ECG interpretation - Narrow complex (QRS width ≤ 90ms) Tachycardia:
 Differentiate between Sinus Tachycardia and Supraventricular Tachycardia
Sinus Tachycardia Supraventricular Tachycardia
P wave present and normal History of abrupt onset
RR interval may vary but PR interval constant P wave absent or abnormal, RR interval constant
Rate: Rate:
Infant: < 220 beats per min Infant: ≥ 220 beats per min
Child: < 180 beats per min Child: ≥ 180 beats per min
4. Sinus tachycardia diagnosed - find and treat causes like hypovolaemia, fever, seizures and consid-
er medical history. Transport to the closest most appropriate medical facility.
5. Supraventricular tachycardia:
 Assess hemodynamically stable (Hypotension, Acute altered mental status and signs of shock)
Stable Mildly Unstable Unstable
Alert and haemodynami- Alert but confused with shortness of Decreased LOC (lethargic to uncon-
cally stable (no signs and breath, chest discomfort and some scious), hypotensive and/or pre-arrest
symptoms, only complains of signs of compensated shock (slight
palpitations) delayed capillary refill and cold periph-
eries)
Transport stable patient with- Attempt vagal stimulation: Valsalva Immediate synchronized cardioversion
out intervention manoeuvre (blow on 10ml syringe) (if time, consider sedation) – 1.0J/kg.
If failed increase to 2.0J/kg
Consider Adenosine: IV/IO – 2 syringes

via 3-way stop
Administer adenosine rapidly followed
by ≥ 5 ml flush
Consider Second dose:
Adenosine: IV/IO – 2 syringes via
3-way stop
Amiodarone can be considered if
adenosine is ineffective. If the child
presents with signs of decompensated
shock proceed to synchronised cardio-
version immediately.
6. ECG interpretation – Wide complex (QRS width ≥ 90ms) Tachycardia diagnosed on ECG:
 Assess haemodynamically stable (Hypotension, acute altered mental status and signs of
shock)
Stable Mildly Unstable Unstable
Alert and haemodynamically Alert but confused with short- Decreased LOC (lethargic to uncon-
stable (no signs and symptoms, ness of breath, chest discomfort scious), hypotensive or pre-arrest
only complains of palpitations) and some signs of compensated
shock (slight delayed capillary
refill and cold peripheries)
Transport stable patient without Consider pharmacological con- Immediate synchronized cardio-
intervention version: version (if time, consider sedation)
– 1.0J/kg.
Amiodarone: (over 30 minutes)
If failed increase to 2.0 J/kg
7. Change to cardiac arrest protocol, if patient becomes pulseless.
CPG 13.8
MANAGEMENT OF PAEDIATRIC AND

NEWBORN HYPOGLYCAEMIA
MANAGEMENT AIM
To recognize hypoglycaemia, in newborns and paediatric patients and to correct the blood sugar level
using either, oral or intravenous carbohydrate therapy as appropriate. The clinical indicators which
1. Recognize the signs and symptoms of hypoglycaemia and a RBS level indicative of hypoglycae-
mia in the two different patient groups.
2. Early administration of appropriate carbohydrate therapy via the most appropriate route of admin-
istration.
3. Repeat the RBS measurement 5 minutes after corrective measures.
1. Identify hypoglycaemia (RBS ≤ 2.5 mmol/l) in newborns. Most neonates are asymptomatic but
signs and symptoms of neonatal hypoglycaemia may include seizures, jitter, high pitch crying, poor
feeding, lethargy or floppy, tachypnoea or apnoea, cyanosis.
2. Identify hypoglycaemia in a Paediatric patient (RBS < 4 mmol/l):
2. In patients with a decreased level of consciousness: Open, clear and maintain the airway. Consid-
er placing the child in neutral, sniffing position or turning lateral, to maintain the airway. Monitor the
airway to ensure that it remains clear.
3. In newborns with hypoglycaemia consider:
 Newborns that are alert, awake and well: Encourage the mother to breastfeed and reassess
RBS if necessary. Alternatively, give oral dextrose (NB: give small amounts on a gloved finger,
do not administer to any neonate with a decreased level of consciousness)
 Newborns with decreased LOC – administer IV 10% dextrose and repeat RBS, 5-10 minutes
after corrective therapy
4. In paediatrics with hypoglycaemia consider:
 In a cooperative paediatric patient administer oral dextrose.
 In an unconscious paediatric patient, administer IV 10% dextrose. Administer this over 5 - 10
minutes monitoring the RBS. Avoid causing hyperglycaemia.
 If unable to obtain IV access and Glucagon is available, administer 1mg Glucagon IM for
patients >20kg (or >6 years old); or 0.5 mg for patients <20kg (or <6 years old). Not for
neonates. CCP scope only.
CPG 13.9
MANAGEMENT OF PAEDIATRIC TRAUMA
MANAGEMENT AIM
To understand the differences in anatomy, physiology and psychological response in paediatrics com-
pared to adults in trauma. Undertake paediatric focused patient assessment and specific trauma care.
1. Recognition of differences which may lead to life threatening complications of trauma.
2. Appropriate patient assessment.
3. Appropriate trauma care for the paediatric patient.
1. Follow the basic principles of CPG 13 Clinical Approach to the paediatric patient while focusing on
identifying life-threatening injuries, providing intervention critical to survival or preventing further
deterioration while prioritizing rapid transportation to an appropriate facility.
2. Consider the C-ABC (Catastrophic hemorrhage control, Airway, Breathing Circulation) to identify
and provide appropriate intervention for life-threatening conditions. Control of significant hemor-
rhage must occur earlier in to increase survival chances. Children have a smaller blood volume
(80-90ml/kg). Their cardiovascular system is able to compensate better for blood loss but when
hypotension occurs it is normally a pre-terminal sign.
1. Immediate control of any severe or catastrophic haemorrhage.

2. Initial assessment: undertake a rapid assessment of the history and mechanism of injury. Do a
quick trauma survey looking for signs of head injury, breathing problems, internal bleeding (chest
and abdomen) and major fractures. Consider spinal injuries and initiate manual spinal immobiliza-
tion by holding the head and neck still.
3. Obtain base line vital signs (pulse rate, respiratory rate, SpO2, BP, GCS, and temperature).
Check RBS if there is an altered level of consciousness.
4. Institute appropriate basic airway maneuvers. Clear the airway (suction) and consider transporting
the patient in a lateral position with spinal consideration. If the pediatric has a compromised airway,
significant facial injury or is unable to maintain their airway due to swelling and SpO2 is compro-
mised despite supplemental oxygen and assisted ventilation then consider surgical airway.
5. Initiate oxygen (CPG 3.3) therapy with one of two options: Use a non-rebreather mask if the
patient is breathing adequately or bag-valve-mask (BVM) assisted ventilation if poor ventilation
present. The aim of supplemental oxygenation is to increase the patient’s SpO2 ≥ 95%.
6. Establish an IV line or insert an I/O if significant trauma is present. Consider procedural sedation
(CPG 13.9) in the awake paediatric patient to reduce the anxiety when undertaking painful proce-
dures.
7. Assess the chest for signs of tension pneumothorax. If present decompress the chest (2nd inter-
costal space midclavicular line).
8. Manage all external bleeding. Administer intravenous fluids if signs of shock are present – give up
to 10-20 ml/kg of normal saline followed by re-assessment of the vitals. If the first fluid bolus fails
to restore adequate circulation then administer a second bolus of 10-20 ml/kg. If internal bleeding
is suspected initiate urgent transport to hospital – priority 1 with pre-notification.
9. Assess the child for pain level. If pain is present administer analgesia (CPG 6.1) as per the pain
guideline.
10. Special considerations:
 Traumatic Brain Injury (TBI): Clear and maintain airway and anticipate vomiting. Monitor SpO2
and End Tidal CO2 to ensure appropriate oxygenation (≥ 95%) and prevent hypoventilation.
» Ensure appropriate fluid resuscitation as hypoperfusion of the brain will lead to second-
ary brain injury. The target blood pressure to maintain the minimum cerebral perfusion
pressure necessary to meet cerebral metabolic demands in infant and children is not well
established. Aim to maintain a systolic blood pressure above the fifth percentile for the age.
» Monitor and avoid hyper/ hypothermia and hyper/ hypoglycemia.
» Ensure adequate analgesia even in patients with decreased level of consciousness.
» In the event of seizures administer Midazolam.
» Aim to ensure venous drainage by maintaining the head in a neutral position and avoid
tightly applied c-collars. There is insufficient evidence to support head elevation in paediat-
rics.
 Burns:
» Stop the burning process and remove all burnt clothing and jewelry unless adhered to
the skin. Chemical: Wet chemical may require irritation whereas dry chemical should be
brushed from the skin.
» Cover the burn wounds with burnshield dressings and prevent hypothermia.
» Establish intravenous therapy and consider fluid bolus if signs of shock.
» Manage pain appropriately.
11. Package the patient according to injuries and mechanism of injury. Use paediatric specific immo-
bilization devices where possible. Appropriately splint all long bone fracture with SAM splint and
consider that application of a traction splint to femur fractures.
PAEDIATRIC TRAUMA CARDIACT ARREST
CPG 13.10
MANAGEMENT OF SHOCK IN
PAEDIATRICS
MANAGEMENT AIM
To recognize inadequate tissue perfusion (shock), identify potential cause and initiate appropriate
intervention. The clinical indicators which suggest the aim is being achieved are the following:
2. Aim to restore or improve tissue oxygenation and perfusion (capillary refill improvement, change in
skin color, increase strength of peripheral pulses, improvement of mental status)
3. Continuous monitoring and re-assessment after fluid resuscitation to prevent and identify fluid
overload.
4. Transport promptly to the closest most appropriate medical facility, with pre-notification.
1. Differentiate between the types of shock and appropriate treatment recommendations:

 Hypovolemic shock:
» Hypovolemic shock is the most common type of shock in paediatric patients which occurs
when the intravascular blood volume decreases resulting in a deceased venous return,
adversely effecting cardiac output and causing inadequate tissue perfusion. Hypovolemic
shock can either be haemorrhagic (commonly secondary to traumatic injuries) or non-hae-
morrhagic (for example secondary to gastrointestinal fluid loss like diarrhoea).
» Clinical features:
 Haemorrhagic: altered mental status, tachycardia, pallor, delayed capillary refill, mot-
tled skin color, cold peripheries (feet and hands), weak peripheral versus central puls-
es, hypotension is a late sign of shock
 Non-haemorrhagic: Above signs and symptoms including signs and symptoms of
dehydration – sunken eyes, sunken fontanelle, dry mucous membranes, lack of tears,
thrust, poor skin turgor, decreased urine output.
 Distributive shock:
» Distributive shock is a state of tissue blood flow maldistribution due to decreased system-
atic vascular resistance. This type of shock includes anaphylaxis, neurogenic shock and
septic shock. Septic shock often manifests elements of distributive shock (abnormal vascu-
lar tone and maldistribution of blood flow) as well as hypovolemia (relative or absolute) and
cardiogenic shock (myocardial dysfunction) along with other complicating factors such as
acidosis, capillary leaking and metabolic imbalances.
» Clinical features of distributive shock typically include flushed skin, tachycardia, and warm
extremities with bounding pulse. Neurogenic (rare in paediatrics) shock secondary to spinal
injury may be accompanied with other traumatic injury and will include flaccid paralysis of
extremities and loss of sympathetic tone (bradycardia, hypotension, warm dry skin, respira-
tory difficulty or arrest). Anaphylaxis may be accompanied by hives, angioedema, pruritus,
tachypnea, stridor, wheezes, and signs of respiratory distress.
» Septic shock can present as cold shock (low cardiac output state) or warm shock (hyperdy-
namic state with high cardiac output and vasodilation). Generally septic shock will present
with a history of recent infection or signs of a local infection with or without fever. Cold
shock present with tachycardia, altered mental states, cold peripheries with weak peripher-
al pulses, mottled skin and delayed capillary refill whereas warm shock present tachycar-
dia, bounding pulses, flushed skin and a brisk capillary refill. With the progression of septic
shock patients can move from a high cardiac output to a low cardiac output, rapidly.
 Cardiogenic shock:
» Cardiogenic shock is caused by a state of decreased myocardial contractility causing
significant decreased cardiac output. It is frequently caused by a state of decreased myo-
cardial contractility like, congenital heart disease, acquired/ ischemic (cardiomyopathies,
infectious myocarditis, hypoxia, overdose, sepsis), metabolic (acidosis, hyperkalemia, etc.)
and trauma. Cardiogenic shock can also be caused by arrhythmias (profound bradycardia,
supraventricular tachycardia or ventricular tachycardia).
» Clinical features: Altered mental status, tachycardia, cold peripheries with weak pulses
and mottled skin color, decreased urine output, jugular vein distention, dyspnea with pul-
monary edema, peripheral edema and hepatomegaly. Hypotension is a late and ominous
sign.
 Obstructive shock:
» Obstructive shock is uncommon in pediatric patients. This type of shock is caused by
extrinsic forces on intrathoracic structures causing decreased cardiac output despite
adequate intravascular volume and normal myocardial contractility. Common causes are
tension pneumothorax, hemopneumothorax, cardiac tamponade.
» Clinical features will include altered mental status, tachycardia, cold peripheries, delayed
capillary refill as well as signs and symptoms of the underlying cause.
2. Check RBS and correct hypoglycemia if present.
3. Do not allow hypothermia. Keep patient warm.
1. Initial assessment: As per CPG 13: Clinical Approach to the Paediatric Patient.
2. Haemorrhagic shock: Stop all obvious external bleeding, initiate fluid resuscitation with 10ml/kg
of 0.9% normal saline over 5-10 minutes, continuously monitor and reassess for improvement of
oxygenation and perfusion after bolus, repeat if necessary to a maximum of 60ml/kg.
3. Distributive Shock:
 Anaphylaxis: reference to CPG 13.4
 Neurogenic shock: Ensure appropriate spinal immobilization, identify and manage respiratory
complications secondary to high spinal injuries.
 Septic shock: Goal is to restore optimal organ perfusion, oxygenation, and mental status. Iden-
tify and correct hypoglycemia with 10% dextrose solution.
 Initiate fluid resuscitation with 20ml/kg of 0.9% normal saline over 5-10 minutes, continuous-
ly monitor and reassess for improvement of oxygenation and perfusion after bolus, repeat if
necessary to a maximum of 60ml/kg. If fluid refractory consider inotropic infusion (Adrenaline or
Epinephrine).
4. Cardiogenic Shock: Treat very cautiously and transport promptly: Consider 5ml/kg fluid bolus with
close monitoring and/or inotropic support (Adrenaline/ Epinephrine). If secondary to arrhythmias,
manage the underlying arrhythmia (refer to CPG 13.7)
5. Obstructive Shock: treat the underlying cause; for example, chest decompression for tension
pneumothorax and consider fluid resuscitation (10ml/kg to a maximum of 60ml/kg) for accompany-
ing hypovolaemia.
PAEDIATRIC FLUID BOLUS
Weight Total max fluid: 60 ml/kg

(kg) 10 ml/kg 20 ml/kg
3 30 ml 60 ml
4 40 ml 80 ml
5 50 ml 100 ml
6 60 ml 120 ml
7 70 ml 140 ml
8 80 ml 160 ml
9 90 ml 180 ml
10 100 ml 200 ml
12 120 ml 240 ml
14 140 ml 280 ml
16 160 ml 320 ml
18 180 ml 360 ml
25 250 ml 500 ml
28 280 ml 560 ml
31 310 ml 620 ml
34 340 ml 680 ml
37 370 ml 740 ml
40 400 ml 800 ml
43 430 ml 860 ml
CPG 13.11
PAEDIATRIC PAIN MANAGEMENT
MANAGEMENT AIM
To appropriately assess and interpret the signs of pain, in order to implement effective control of pain.
1. Conduct a pain assessment.
2. Recognizing signs of pain in the paediatric patients.
3. Initiate pain management to prevent suffering and clinical deterioration.
1. Initial assessment: As per CPG 13: Clinical approach to the paediatric patient.
2. Conduct a pain assessment using the FLACC behavioural pain scale for non-verbal paediatrics or
the analogue pain score or Wong-baker Faces Scale (CPG 6.1) for paediatrics willing to talk.
3. As for adult, treat the underlying cause of pain where possible. For example splint fractures to mi-
nimise movement and further trauma and bleeding. Apply burn shield to burns to aid with cooling
and to alleviate pain.
4. Calm and reassure the patient and always keep the patient’s parents informed and involved in the
patient’s management.
5. Non-pharmacological approach to pain management in paediatrics:
 Distract attention from the painful stimuli.
 Keep the patient’s parents calm and involved in the management of their child.
 Positive incentives, particularly from parents.
6. Pharmacological management of pain: Any patient with a pain score of > 4 or experience severe
pain must receive pain relief. Considering that emotional and mental development occurring
during childhood, practitioners must understand that children may not be able to appropriately
communicate and verbalize pain; as a result in light of the patient’s underlying clinical condition,
practitioners must anticipate pain. Remember that a patient with a decreased level of conscious-
ness can still experience pain and pain management in these patients must be considered. Always
exclude contra-indication of medication prior to administration:
 Penthrox – Inhalational analgesia should be considered in the pain management of paediatrics
provided the child is sufficiently developed to understand instruction and self-administer the
medication. (AP/CCP)
 Oral analgesics – Paracetamol can be used in mild to moderate pain for example: headaches,
minor trauma like soft tissue injuries, minor burns, sprains and strains etc. (AP/CCP)
 Parenteral analgesics:
» IV Paracetamol – this drug is an appropriate option for patients with mild to moderate pain
when the oral dose is not possible. In patients presenting with pain which is not severe
enough to administer either Fentanyl or Ketamine, Paracetamol IV should be considered
as it has a lesser side effect profile with no sedatory properties. It has been shown to be as
effective as morphine in moderate pain management. Do not use if Paracetamol adminis-
tered in the last 4-6 hours. (CCP)
» Fentanyl – this is the gold standard opioid and is approved for use by critical care para-
medics. When administering Fentanyl, Naloxone must be available at all times. Anti-
emetics should not be used prophylactically following the application of opioids. They
should be administered only if nausea and vomiting occur. Opioid induced nausea at the
time of administration is usually related to the speed of injection. (CCP)
» Ketamine is a non-opioid, parenteral analgesic that at higher doses is a general anaesthe-
sia agent. It is particularly useful in cases of trauma and burns because it does not cause
significant cardiovascular or respiratory depression. Patients may experience unpleasant
“emergence phenomena”. It may cause increased salivation, so careful airway manage-
ment is important. (CCP)
» Re-assess pain score 5-10 minutes after analgesia administration.
» Continuously monitor the patient’s level of consciousness and vital signs during transporta-
tion to hospital. Closely monitor for adverse effects.
Certain medications for the management of pain such as Penthrox, Fentanyl, Midazolam and Ket-
amine can result in sedation of the patient which may result in the loss of protective airway reflexes or
ability to independently maintain adequate ventilatory function. These effects are often unpredictable
and can be specific to the individual, regardless of the dose administered. Staff should be prepared to
appropriately monitor for and manage sedation levels deeper than what was intended. For this reason
the following monitoring requirements, in addition to regular assessment of the basic vital signs (HR,
RR, BP, and LOC), should be followed as a minimum standard:
1. Equipment for the monitoring of vital signs including ECG, RR, BP, EtCO2 and/ or SpO2 must be
immediately available.
3. ECG and SpO2 must be continuously monitored any time the patient receives narcotics, benzodi-
azapines, or dissociative agents by any route.
4. If narcotics and benzodiazapines are administered to the same patient, continuous EtCO2 monitor-
ing is required.
6. BP should be measured at a minimum of every 5 minutes.
7. For inhaled analgesics (Penthrox) continuous SpO2 and HR monitoring is recommended.
CPG 13.12
PAEDIATRIC PROCEDURAL SEDATION
MANAGEMENT AIM
To provide procedural sedation to paediatric patients prior to any painful or distressing procedures.
1. Paediatric patient is provided adequate sedation to relieve pain/ distress during painful procedure.
2. Sedation does not impact on the oxygenation or haemodynamic status of the child.
Indications for the use of procedural sedation for paediatrics:

 Painful or emotionally disturbing procedures in conscious children less than 14 years of age.
 Consider when initiating IV/IO, splinting fractures or dressing significant soft tissue injuries.
2. Undertake life-saving clinical treatment as per relevant CPG.
3. If procedural sedation is indicated:
 Agent of choice is Ketamine (dissociative sedation with good safety profile) IV or IM/ IN -
dosage choice based on level of sedation required.
 Light sedation: 0.5mg/kg IV/IO or 1-2mg/kg IN/IM
 Deeper sedation: 1-1.5mg/kg IV/IO or 2-4mg/kg IN/IM
 Ketamine has a lower adverse events profile, with no effect on airway (except in paediatrics
less than 3 months old), breathing, or blood pressure. Emergence phenomenon is rare
(Midazolam not shown to reduce emergence phenomenon).
 Ketamine produces both sedation and analgesic effect, and has better efficacy than Midazolam
or Fentanyl combination
4. Contraindications (Ketamine for sedation):
 Age less than 3/12
 Upper respiratory infections (increased risk of laryngospasm).
5. Fasting is not required, incidence of emesis patients extremely low.
6. Always be prepared for a level of sedation deeper than what was intended and have equipment
necessary to provide respiratory and cardiovascular support if required.
1. Equipment for the monitoring of vital signs including ECG, RR, BP, EtCO2 and/or SpO2 must be
immediately available.
3. ECG, SpO2 and EtCO2 must be continuously monitored, regardless of route of administration or
dose.
5. BP should be measured at a minimum of every 5 minutes.
CPG 13.13 PAEDIATRIC RAPID SEQUENCE INTUBATION DRILL
ONLY FOR CHILDREN (≥8 YEARS OLD) SUSTAINING MAJOR TRAUMA
Assessment Considerations Other Considerations
 Is there failure of airway patency/ protection?  Do I have adequate access to the patient?
 Is there failure of oxygenation or ventilation?  Do I have an assistant?
 Do I expect the clinical course to deteriorate?  Do I have a bougie?
 Is this a potentially difficult airway?  Am I able to position for optimal laryngoscopy?
 Do I have a mechanical ventilator readily available?
 Do I have a backup BVM readily available?
for at least 94% SpO2 if possible. Leave EtCO2 nasal cannula in
cannula AND facemask. AVOID ROUTINE USE OF BVM! Aim
Provide at least 3 minutes of pre-oxygenation with EtCO2 nasal
 Laryngoscope (large and small handles) with working

place for apnoeic oxygenation during laryngoscopy.
Prepare equipment, light source and blades

Prepare yourself mentally,
 Tested suction unit with suction catheter
Prepare for difficult/ failed intubation
 Lubricated bougie
 Endotracheal tubes (3 size options available)
 Supraglottic airway device and video laryngoscope in
Position patient 20-25º head-up for readiness
optimal pre-oxygenation and laryngoscopy  Surgical airway kit in readiness
Align the airway axes and place a pad under occiput  Medications (checked and confirmed with partner)
CHILDREN DESATURATE FASTER!  Plan for mechanical ventilation
 Ensure bilateral IV lines are in place
Paralyze and induce the patient

 Run in at least 250ml of Nacl 0.9%
 Administer Fentanyl up to 3mcg/ kg PLUS Ketamine up
to 2mg/kg first then Suxamethonium 2mg/ kg; OR
Perform External Laryngeal  Fentanyl up to 3mcg/ kg PLUS Ketamine up to 2mg/ kg
first, then Rocuronium 1-1.5mg/ kg.
Manipulation and/ or BURP
techniques as required  For hemodynamically unstable patient reduce to
Fentanyl 1mcg/ kg PLUS Ketamine 1mg/ kg. Rocuronium
OR Suxamethonium dose remains the same.
 Check for jaw flaccidity before attempting laryngoscopy.
Place the ETT in the trachea and

confirm correct position
 Use a bougie or video laryngoscope for the primary
attempt.
 Visualize the ETT go through the vocal cords.
Post-intubation  Auscultate EPIGASTRIUM/ LEFT LUNG/ RIGHT LUNG
management  Confirm capnography waveform – apply oesophageal
detector device
 Secure ETT with commercial device and note the mark-

ing at the teeth level.
 Ensure that the ETT cuff is adequately inflated.
 Place the patient on a mechanical ventilator as soon as
practically possible. Continuously monitor EtCO2
Maintain sedation and paralysis
 Ketamine 0.25 - 0.5mg/ kg every 15 - 20 min. as neces-
sary
 Fentanyl 0.5mcg/ kg as needed
 Rocuronium 1mg/ kg within 6 - 8 minutes of initial Sux
 Consider passing a gastric tube to decompress stomach
AP & CCP CCP

 Always prepare as if the airway is going to be difficult!
CPG 13.13
RAPID SEQUENCE INDUCTION

FOR PAEDIATRICS
MANAGEMENT AIM
The clinical decision making, indications, procedure, and management aim of RSI in the paediatric
population is the same as is in the adult population (see CPG 2.3).
1. This CPG is aimed at children who fall into the age category 8-14 years old who have experienced
major traumatic injuries. Patients older than 14 years should be treated as adults.
2. RSI is NOT permitted in children less than 8 years old.
3. RSI is NOT permitted in children that require endotracheal intubation as a result of a medical
(non-trauma) event.
4. RSI in children is permitted ONLY IF:
 The child to be intubated is presumed to be* 8 years or older AND;
 Has sustained trauma leading to the need for endotracheal intubation.
5. A minimum standard of SpO2, EtCO2 and 4-Lead ECG monitoring is advocated in ALL paediatric
intubations. A blood pressure should be measured at least every 5 minutes during and after the
RSI procedure, until delivery to hospital.
6. When estimating paediatric weight, equipment sizes and drug dose calculations, refer to the
HMCAS Paediatric Treatment Reference Guide and/ or dose formulary within Clinical Practice
Guidelines.
* HMCAS accepts that the estimation of age is challenging in the pre-hospital environment where
English is not a first language of the majority of our patients.
The INDICATIONS and CONTRAINDICATIONS for paediatric RSI are the same (CPG 2.3).
1. PREOXYGENATION
NOTE: Children desaturate at a much faster rate than adults! Therefore remember to adequately
pre-oxygenate the paediatric patient.
Preoxygenation is designed to increase the reserves of oxygen within the lungs by denitrogenation of
the functional residual capacity (FRC). This prolongs the apnoeic period before hypoxaemia ensues.
Maintenance of a patent airway during the apnoeic period allows oxygen to reach the alveoli by the
process of bulk flow. This occurs as a result of differences in the volume of oxygen consumption and
CO2 production and their respective solubility in blood. Oxygen administered by nasal prongs together
with a facemask, with a patent airway, prolongs the time to desaturation. Owing to the negative pres-
sure gradient that bulk flow causes, it is important to maintain the application of continuous positive
airway pressure via a tight fitting mask, in order to reduce atelectasis. This is emphasized in children,
as they are more prone to atelectasis and hypoxaemia on induction because of the combination of a
reduced FRC, increased closing volume, and higher respiratory rate.
Avoid routine use of the bag-valve-mask (IPPV) as a means of pre-oxygenation. The BVM increases
the risk of gastric insufflation and regurgitation during/after the procedure. When possible, pass a
gastric tube to decompress the stomach with due consideration of the time-critical nature of trauma.
2. POSITIONING DURING PREOXYGENATION

In adults, pre-oxygenation may be best achieved with the patient in a 20-25° head up position. This
has been shown to improve efficacy and consequently produce an increased time to desaturation.
Although such an effect is unproven in the paediatric population, it would seem sensible to consider its
use more frequently in children.
3. RECOMMENDED MEDICATION ADMINISTRATION

FIRST LINE: PRIMARY INDUCTION AND PARALYSIS
1. Administer INDUCTION agent followed by saline flush
 STABLE PATIENTS (Blood pressure within normal age-range)
» Fentanyl up to 3mcg/kg
» Ketamine up to 2mg/kg
 UNSTABLE patients (Severe hypotension)
» Fentanyl 1mcg/kg
» Ketamine 1mg/kg
2. Administer Suxamethonium 2mg/ kg. If Suxamethonium is contraindicated, then administer Rocu-
ronium 1-1.5mg/kg IVI
Anaesthesia for RSI and ventilation requires the three components of hypnosis, analgesia and paraly-
sis. Depending on the patient’s condition and pathology individual parts of the diagram below may
have to be altered (see CPG 2.3).
The objective is to prevent awareness and maintain ‘haemodynamic stability’. Hypotension in brain
injury is harmful. A child with low GCS and normal to high blood pressure due to traumatic brain injury
will need less hypnosis but increased analgesia and paralysis.
A child with a low blood pressure but conscious will need hypnosis and paralysis but analgesia can be
reduced. Invariably the practitioner will have to make some trade-off decisions and although a ‘Recipe
Approach’ provides some degree of safety, adjustments will have to be made on a case by case basis.
Ensure that the patient is given adequate sedation, analgesia and continuous neuromuscular block-
ade after confirming placement of tracheal or supraglottic airway device. Place the patient onto a
mechanical ventilator as soon as possible to minimize variations/ derangements in ventilation.
CPG 14.1
CONTINUATION OF PREVIOUSLY
PRESCRIBED MEDICATION
MANAGEMENT AIM
Critical Care Paramedics (CCP) may be required to move patients, between healthcare facilities, with
medication infusions not included within their current pharmacopeia and without the support of escort-
ing medical staff. Critical Care Paramedics may comply with this request to meet patient needs where
the following is achieved or met:
1. It is in the patient’s best interest that the medication is continued during transportation. Stopping
the medication, for transportation, is not a viable option.
2. That due consideration to transferring the patient via SHAARP.
3. The attending Critical Care Paramedic is happy to transfer the patient and has discussed the
transfer with silver clinical.
4. That the medication has been prescribed by a QCHP licensed doctor or by a doctor entitled to
work within Qatar (e.g. US military doctors) and that the prescribing doctor has continued respon-
sibility for the prescribed medication (as is the case when prescribed within a static healthcare
facility)
The primary aim of this CPG is to facilitate safe, effective transportation of patients who are receiving
medication not included within the CCP’s current pharmacopoeia. This CPG is designed to be flexible
to reflect the wide scope of potential requests and the variable experience of CCP’s.
Choice/ list of medications:
There are no drugs that are exempted by this policy on the understanding that the following criteria
are met:
1. The medication is required for the safe and/ or optimal transportation of the patient.
2. The medication is prescribed by the referring doctor AND the CCP has had an opportunity to re-
view the prescription.
 The referring doctor may prescribe a dosing range if required for the CCP to follow.
 The referring doctor may prescribe a fixed dose for the CCP to follow.
3. That the referring doctor understands that they remain the responsible clinician for any medication
that they prescribe that falls outside of the CCP’s normal pharmacopeia that the attending clini-
cian’s wishes continued during the transfer
4. That the CCP is happy to transfer the patient and CCP understands that they are empowered to
discontinue the medication should an adverse event occur.
Whilst the referring doctor retains responsibility for the prescription of any medication outside of the
CCP’s standard pharmacopeia the attending CCP is responsible for ensuring optimal patient safety
during transportation. Therefore, the following steps are recommended:
1. Confirm that the medication is required for the ongoing management of the patient routine infu-
sions such as hydration fluids (excluding burns) should, where feasible, be discontinued during
elected transportation
2. If the CCP believes that an alternative medication, within their pharmacopeia, is an option then this
should be raised with the referring doctor
3. Access the HMCAS Transfer and Retrieval Service extended pharmacopeia (available on the
ePCR under CPG’s) as the requested drug may be listed within this pharmacopeia providing ad-
vice and support on drug administration and appropriate dosing regimes.
4. Silver clinical should be informed of the request to continue medication that is outside of the CCP’s
pharmacopeia. If conflict exists as to the appropriateness/safety of the medication, then the trans-
fer should be delayed until the referring hospital can supply an appropriate escort or until such
time that the medication is no longer required.
Actions once continuation of previously prescribed medication during transportation has been
agreed:
1. The CCP should review the prescription noting the dose and/or dose range prescribed at the host
medical facility
2. The medication and the dose range along with the referring doctors name should be entered into
the CCP’s ePCR.
3. The medication should be reviewed to ensure that:
 Its compatible with syringe driver or infusion pumps carried by the CCP
» Where the current medication is not compatible then either: a) a new infusion is drawn up
using compatible syringes or b) the current infusion pump is continued during transporta-
tion. Option B is the least viable option and requires the following:
 CCP must be familiar with the infusion device
 There is adequate battery life for the duration of the transfer plus 60 minutes OR the
device is chargeable within the transferring ambulance
 That the referring hospital understands that the ambulance service can not ensure the
timescale for the return of the infusion device
» That the CCP understands the dosing range and the concentration of the medication
» That there is adequate medication provided to cover the transfer at the maximum pre-
scribed infusion rate with the addition of at least an additional 60 minutes of infusion time.
Action on adverse reaction to ongoing medication:

1. Treat anaphylaxis and/or hypotension as per standard CPG’s
2. Discounted medication
3. Ensure adverse event is documented in an HMCAS OVA and handed over to receiving healthcare
facility
CPG 14.2
USE OF SPECIALIST MEDICATION

DURING TRANSFER
MANAGEMENT AIM
The aim of this CPG is to facilitate level two and three transfers led by CCP’s supported by on-call
senior clinicians and forms part of the privileges of transferring critical care paramedics. To this end a
group of drugs (extended pharmacopeia Transfer and Retrieval Services) are available for use during
inter-facility transfers. The utilization of these medications is limited to CCP following direct consulta-
tion with silver clinical and/ or MICU consultant.
The list of medication within the extended pharmacopeia Transfer and Retrieval Services may be uti-
lized during transportation of patients following on-line consultation. The decision on what drug is best
suited for the transfer is subject to online consultation between the attending critical care paramedic
and silver clinical and/ or MICU consultant.
 Treatment protocol is agreed with the on-call clinician (adhere to SOP – verbal orders)
 Treatment protocol is by the attending CCP within the transfer record
As per instruction from silver clinical or on-call ICU consultant.
FORMULARY
HMCAS CLINICAL PRACTICE GUIDELINES Version 1.4 2019 FORMULARY PAGE 243
Weight calculations for
adults and paediatrics
Many of the drug regimens require the administration of a weight-based dose. In HMCAS we will work
on ideal body weight rather than actual body weight (especially in circumstances where the adult
patient or parents/care giver of a paediatric patient are unable to provide a recent weight). Thus the
estimation of the patient’s ideal body weight needs to be made. This is carried out as follows:
ADULT IDEAL BODY WEIGHT FORMULA:
Measure the patient’s height (in centimeters) using a tape measure. Then apply the following formula:
Height (cm) – 100 = ideal body weight (Add or Subtract up to 20% for larger or smaller patients)
PAEDIATRIC IDEAL BODY WEIGHT FORMULA
Estimate weight calculations:

0 – 12 months: (age x 0.5) + 4
1 – 5 years: (age x 2) + 8
6 – 14 years: (age x 3) + 7
Finger counting method1: works to 9 yrs old

Start from the thumbs
Left thumb = 1yr old and Right thumb = 10kgs
Each finger then represents + 2yrs in age and
+ 5kgs in weight
For even years use average weight between two
fingers (eg. 10kg and 15kg – average is 12.5kg)
1
Young TP, Chen BG, Kim TY, Thorp AW, Brown L. Finger Counting: an alternative method for estimating pediatric weights. American Journal of Emergency Medicine: 2013.
PAEDIATRIC WEIGHT CALCULATIONS
Age in months Weight in kg
Weight in kg Age in Years
[(age x 0.5) + 4] [(age x 2) + 8]
Birth 3 - 3.5 1 year 10
1 Month 4.5 2 years 12
2 Months 5 3 years 14
3 Months 5.5 4 years 16
5 Months 6.5 Age in Years [(age x 3) + 7] Weight in kg
7 Months 7.5 7 years 28
8 Months 8 8 Years 31
9 Months 8.5 9 Years 34
11 Months 9.5 11 Years 40
Adenosine
PHARMACOLOGY
Class
Antiarrhythmic
Action
Slows AV conduction time and is therefore able to interrupt re-entry circuits through the AV node, thus
restoring normal sinus rhythm in patients experiencing paroxysmal SVT, including PSVT associated
with WPW (Wolff-Parkinson-White Syndrome).
Metabolism
 Adenosine is rapidly cleared from the circulation via cellular uptake.
 Requires no hepatic or renal function to be activated or inactivated.
Primary Emergency Indications
Symptomatic SVT (narrow complex <0.12 s.)
Contraindications
 Known hypersensitivity to Adenosine
 Second or third degree heart block
 SSS (Sick sinus syndrome)/ sinus node disease
 AF with accessory pathways (Wolf-Parkinson-White syndrome)
Precautions
Use with caution in patients:
 With asthma (due to mast cell degranulation and histamine release)

 With patients with obstructive lung disease not associated with bronchoconstriction.
 On Digoxin, or Digoxin and Verapamil. There have been instances of prolonged asystole, some
cases of which have been fatal.
Route of Administration
 IV – antecubital fossa site is preferred due to their proximity to the heart.
 External Jugular
 Humeral head IO
Side Effects
 Bradycardia
 Hypotension
 Facial flushing
 Chest pressure
 Shortness of breath
Special Notes
 The half-life of Adenosine is < 10 seconds. Thus, adverse effects are generally self-limiting
 Varying arrhythmias may present at the time of conversion to sinus rhythm (seen in 55% of pa-
tients). These are usually self-limiting and do not require intervention.
 Half life = <10 seconds
 Draw up Adenosine in a 5ml syringe, and 20mls of saline in another syringe. Attach both syringes
to the IV via a 3-way TAP. Administer the Adenosine rapidly and follow immediately with the 20ml
bolus of saline.
ADENOSINE DOSAGE
ADULT
 6mg RAPID IV push
 Repeat once: 12mg RAPID IV push if required.
PAEDIATRIC
 0.1 mg/kg RAPID IV push – maximum dose 6mg
 Can repeat 0.2 mg/kg RAPID IV push once only – maximum dose 12mg
PAEDIATRIC SUPRAVENTICULAR TACHYCARDIAS
Weight 1st Dose IV Volume 2nd Dose IV Volume

(0.1 mg/kg) (0.2 mg/kg)
Drug concentration: 3 mg/ml – Max first dose 6 mg, Max second dose 12 mg
3 kg 0.3 mg 0.6 mg 0.2 ml
0.1 ml
4 kg 0.4 mg 0.8 mg
0.3 ml
5 kg 0.5 mg 1 mg
6 kg 0.6 mg 0.2 ml 1.2 mg 0.4 ml
7 kg 0.7 mg 1.4 mg
0.5 ml
8 kg 0.8 mg 1.6 mg
9 kg 0.9 mg 0.3 ml 1.8 mg 0.6 ml
10 kg 1 mg 2 mg 0.7 ml
12 kg 1.2 mg 0.4 ml 2.4 mg 0.8 ml
14 kg 1.4 mg 2.8 mg 0.9 ml
0.5 ml
16 kg 1.6 mg 3.2 mg 1.1 ml
18 kg 1.8 mg 0.6 ml 4.6 mg 1.2 ml
25 kg 2.5 kg 0.8 ml 5 mg 1.7 ml
28 kg 2.8 mg 0.9 ml 5.6 mg 1.9 ml
31 kg 3.1 mg 1 ml 6.2 mg 2.1 ml
34 kg 3.4 mg 1.1 ml 6.8 mg 2.3 ml
37 kg 3.7 mg 1.2 ml 7.4 mg 2.5 ml
40 kg 4.0 mg 1.3 ml 8 mg 2.7 ml
43 kg 4.3 mg 1.4 ml 8.6 mg 2.9 ml
Adrenaline/ Epinephrine
PHARMACOLOGY
Class
 A naturally occurring alpha and beta adrenergic stimulant
 Sympathomimetic
Actions
 Increases HR by increasing the S.A. node firing rate (Beta 1 receptors) – at moderate doses
 Increases conduction velocity through the A.V. node (Beta 1 receptors) – at moderate doses
 Increases myocardial contractility (Beta 1 receptors) – at moderate doses
 Increases the irritability of the ventricles (Beta 1 receptors) – at moderate doses
 Bronchodilation (Beta 2 receptors) – at moderate doses
 Peripheral vasoconstriction (Alpha receptors) – at high doses
 Stabilises mast cells (histamine antagonist)
Metabolism
 By monoamine oxidase and other enzymes in the blood, liver and around nerve endings.
 Excreted by the kidneys (mostly in the form of inactive metabolites)
 Anaphylaxis
 Croup
 Cardiac arrest
 Severe respiratory distress, secondary to upper airway swelling
Contraindications
Nil in the setting of a life-threatening emergency.
Precautions
 Elderly patients
 Patients with significant previous cardiac history (including CV disease, hypertension)
 Patient taking monoamine oxidase inhibitors (the effects of Adrenaline/ epinephrine may be po-
tentiated)
 Patients in acute pulmonary oedema may arrest after the administration of Adrenaline/ epineph-
rine due to peripheral vasoconstriction or cardiac stimulation.
 In the situation of cardiac arrest associated with hypovolaemic shock, ensure adequate fluid re-
placement is provided in conjunction with administration of Adrenaline/ epinephrine.
 Intravenous (IV)
 Intramuscular (IM)
 Intraosseous (IO)
 Intravenous infusion
 Nebuliser
Side Effects
 Sinus tachycardia
 Supraventricular arrhythmias
 Ventricular arrhythmias
 Hypertension
 Pupillary dilation
 May increase the size of a myocardial infarction
 Anxiety
 Palpitations
 Cerebrovascular haemorrhage
 Tissue necrosis in the cases of extravasation or repeated IM injections at the same site
Special Notes
 HR, BP and ECG must be continuously monitored
 IV adrenaline/epinephrine should be reserved for life-threatening situations
 Protect ampoules from light
 Adrenaline/ epinephrine 1:1 000 should be diluted when used in the cardiac arrest setting –
preferably use the 1:10 000 preparation
 When administered IM – use a different location each time you administer to avoid local tissue
necrosis
 IV administration
 Onset: 30 seconds
 Duration: 5-10 minutes
 IM administration
 Onset: 5-10 minutes
 Duration: 1-4 hours
 Inhaled
ADRENALINE/ EPINEPHRINE DOSAGE
ADULT
CARDIAC ARREST
 1mg IV/IO
 Repeat every 4 minutes
UPPER AIRWAY OBSTRUCTION (SWELLING)

 5mg in 5ml undiluted (1:1 000) nebulised.
ANAPHYLAXIS / SEVERE ALLERGIC REACTION

 0.5 mg IM
 Repeat every 5 minutes if required.
BRADYCARDIA / INOTROPIC SUPPORT

 2-100mcg/min
 Utilizing Syringe Driver:
 Use 1:10 000 (mix 2mg of 1:1 000 [2 ampules] into 18ml of Normal Saline)
 Start with 2 ml/ hr (3.3 mcg/min) into dedicated cannula
 Measure BP every 2 minutes.
 Increase rate by doubling the previous increment (ie 4ml/hr – 6.6mcg/min etc.)
 Reduce dose by halving the previous increment
If there is not sufficient time to prepare the syringe drive, an emergency interim push-dose can
be initiated.
Push-dose Adrenaline as interim while preparing infusion:

 Draw 1mg (1:1000) and dilute with 9ml NaCl creating a 1:10 000 dilution
 Discard 9ml, leaving 1ml (100mcg)
 Draw up another 9ml NaCl into the same syringe, diluting the 100mcg to 10mcg/1ml
creating a 1:100 000 dilution.
 Administer 1-2ml every 3-5 minutes as required based on BP response while preparing
infusion
PAEDIATRIC
CARDIAC ARREST
 0.01 mg/kg IV/IO
 Repeat every 4 minutes
PAEDIATRIC INOTROPE
 0.05 – 0.3 mcg/kg/min
 Use 1:10 000 (2mg in 18ml Saline)
 See Weight based paediatric drug infusion chart
ANAPHYLAXIS / SEVERE ALLERGIC REACTION

 0.01mg/kg IM for all ages, maximum dose of 0.5mg.
 Repeat every 5 minutes if required
Use IM dose ranges:
 < 6 years: 0.15 mg (0.15 ml)

 6 – 12 years: 0.3 mg (0.3 ml)
 > 12 years: 0.5 mg (0.5 ml)
 Repeat every 5-15 minutes
SEVERE RESPIRATORY DISTRESS
 0.01 mg/kg IM (max dose 0.3 mg)
BRADYCARDIA
 0.01 mg/kg IV/ IO max dose 0.5mg.
 Repeat every 4 minutes as required
CROUP
 0.5mg/kg up to a maximum of 5mg in 5ml nebulised as a single dose.
PAEDIATRIC ADRENALINE DOSAGES
Weight Cardiac Arrest and Bra- Anaphylaxis

dycardia
IV/IO (0.01 Volume IM (0.01 Volume Neb Volume
kg/mg) kg/mg) (0.5mg/
kg)
1 mg/10ml (1:10 000) 1 mg/ml (1:1 000)
3 kg 0.03 mg 0.3 ml 1.5 mg 1.5 ml
4 kg 0.04 mg 0.4 ml 2 mg 2 ml
5 kg 0.05 mg 0.5 ml 2.5 mg 2.5 ml
6 kg 0.06 mg 0.6 ml 3 mg 3 ml
7 kg 0.07 mg 0.7 ml 3.5 mg 3.5 ml
8 kg 0.08 mg 0.8 ml < 6 years 4 mg 4 ml
- 0.15 0.15 ml
9 kg 0.09 mg 0.9 ml mg 4.5 mg 4.5 ml
10 kg 0.1 mg 1 ml
12 kg 0.12 mg 1.2 ml
14 kg 0.14 mg 1.4 ml
16 kg 0.16 mg 1.6 ml
18 kg 0.18 mg 1.8 ml
6 – 12
25 kg 0.25 mg 2.5 ml years – 0.3 ml
0.3 mg
5 mg 5 ml
28 kg 0.28 mg 2.8 ml
31 kg 0.31 mg 3.1 ml
34 kg 0.34 mg 3.4 ml
37 kg 0.37 mg 3.7 ml
40 kg 0.4 mg 4 ml
> 12
43 kg 0.43 mg 4.3 ml years – 0.5 ml
0.5 mg
Amiodarone
PHARMACOLOGY
Class
Class III anti-arrhythmic agent, although possessing characteristics of all 4 Vaughan Williams classes.
Actions
 Blocks myocardial K+ (potassium) channels – leads to slowed conduction and prolonged refrac-
toriness
 It blocks sodium channels
 It has a non-competitive anti-sympathetic action
 It lengthens cardiac action potential
 Negative chronotropic effect in nodal tissue
 It’s vasodilatory action decreases myocardial workload and subsequently myocardial oxygen
consumption
Metabolism
 By the cytochrome P450 enzyme which is present in the liver and the intestines
 Biliary excretion
 Cardiac arrest presenting in VF or pulseless VT
 Rapid AF (atrial fibrillation) or atrial flutter less than 24-hour duration
 SVT (supraventricular tachycardia)
 VT with a pulse
Contraindications
 Hypersensitivity to Amiodarone or Iodine
 Cardiogenic shock
 Second or third degree AVB (AV block)
 Severe sinus node dysfunction
Precautions
 Use with caution in patients taking B-blockers, calcium antagonists or Diltiazem – because of the
possible potentiation of bradycardia, sinus arrest and AV block
 Concurrent administration of Fentanyl and Amiodarone may exacerbate bradycardia, hypotension
and decreased cardiac output.
 Patients with thyroid dysfunction can have an exacerbation of their arrhythmia or death second-
ary to Amiodarone administration. Monitor carefully.
 IV
 IO
Side Effects
 Hypotension (most common side effect)
 Bradycardia
Special Notes
 Must be mixed with D5W – Amiodarone is incompatible with saline.
 Protect from light and excessive heat
 Treat hypotensive episodes secondary to Amiodarone administration by slowing the rate of
infusion (as this is the most common reason for presenting hypotension), and consider volume
replacement concurrently.
 Treat episodes of bradycardia by slowing the rate of Amiodarone infusion – or in severe cases
ceasing it.
 Infusing Amiodarone too quickly can result in liver failure, renal failure and death
 Bolus IV effects
 Onset: 2 minutes
 Peak: 20 minutes
 Duration: 2 hours
AMIODARONE DOSAGE
ADULT
VF/ PULSELESS VT
 300mg IV bolus after third shock
 Repeat 150mg bolus after fourth shock
VT WITH A PULSE / RAPID AF< 24 HOURS DURATION

 300 mg slow IV/IO – over at least 15 minutes
Dilution:
 Ampoule = 150mg in 3 ml
 300mg (i.e. 2 ampoules of 150mg) diluted with 44mls of Dextrose 5% to 50mls in a 50ml
SYRINGE
 Final Concentration is 6mg/ml
 when preparing Amiodarone for bolus administration it is advisable to first draw up 5-10ml
of 5% dextrose (in a 20ml syringe) and then draw up the Amiodarone. This will minimize
the ‘frothing’ that occurs when drawing up Amiodarone.
Dosage:
 200ml/hr (20mg/min) for 15 minutes.
PAEDIATRIC
VF / PULSELESS VT
 5 mg/kg IV/IO – Repeat twice up to 15mg/kg - max dose 300mg
SVT
 5 mg/kg IV over 20-60 minutes, max dose 300mg.
VT WITH A PULSE
 5 mg/kg IV over 20-60 minutes, max dose 300mg.
AMIODARONE
Cardiac Arrest (VF and pVT), Narrow and Wide complex tachycar-
dia (20 – 60 minutes)
Weight
IV/IO (5 mg/kg) Volume
Concentration: 150 mg/3 ml
3 kg 15 mg 0.3 ml
4 kg 20 mg 0.4 ml
5 kg 25 mg 0.5 ml
6 kg 30 mg 0.6 ml
7 kg 35 mg 0.7 ml
8 kg 40 mg 0.8 ml
9 kg 45 mg 0.9 ml
10 kg 50 mg 1.0 ml
12 kg 60 mg 1.2 ml
14 kg 70 mg 1.4 ml
16 kg 80 mg 1.6 ml
18 kg 90 mg 1.8 ml
25 kg 125 mg 2.5 ml
28 kg 140 mg 2.8 ml
31 kg 155 mg 3.1 ml
34 kg 170 mg 3.4 ml
37 kg 185 mg 3.7 ml
40 kg 200 mg 4.0 ml
43 kg 215 mg 4.3 ml
Aspirin (acetylsalicylic acid)
PHARMACOLOGY
Class
Prostaglandin inhibitor
Action
 Analgesic (through inhibition of prostaglandin synthesis)
 Antipyretic (through promotion of vasodilation and sweating by acting on the brain’s heat regulat-
ing centre)
 Anti-platelet aggregation agent - reduces platelet aggregation
 Anti-inflammatory action is through inhibiting the synthesis of prostaglandins
Metabolism
 Converts to salicylate in the gut mucosa and liver
 Excreted mainly by the kidneys
To minimise platelet aggregation and thrombus formation in order to retard the progression of coro-
nary artery thrombosis in the patient with acute coronary syndrome
Contraindications
 Hypersensitivity to aspirin/salicylates/NSAIDS
 Actively bleeding peptic ulcers
 Bleeding disorders (EG: haemophilia)
 Suspected dissecting aortic aneurysm
 Pregnancy
Precautions
 Peptic ulcer
 Asthma (patients with a history of asthma have an increased risk of having a hypersensitivity
reaction)
 Patients on anti-coagulant therapy (eg: Warfarin)
 Reye Syndrome has been associated with children and teenagers with febrile illness
 Patients with impaired liver function may develop hepatotoxicity
Oral
Side Effects
 Heartburn
 Gastrointestinal bleeding
 Hypersensitivity reactions
 Dizziness/tinnitis
Special Notes
 Half-life of Aspirin is 2 - 4.5 hours
 Do not delay the administration of ASA to obtain a 12-Lead in suspected ACS
DOSAGE
ADULT
 300mg tablet chewed
 may still be administered to patients receiving oral anticoagulation if a STEMI is con-
firmed.
 aspirin at the full dose of 300mg can still be administer even to those patients who
receive regularly prescribed aspirin.
Atropine
PHARMACOLOGY
Class
Anti-cholinergic/ anti-parasympathetic agent and muscarinic antagonist.
Action
 Blocks Ach (acetylcholine) receptors at the neuro-effector site
 Increases HR by increasing S.A. node firing rate
 Increases conduction velocity through the A.V. node
 Acts as an antidote to reverse the effects of cholinesterase inhibitors
Metabolism
 Metabolised by the liver
 Excreted by the kidneys (up to 50% in its unchanged form)
 Bradycardia
 Organophosphate poisoning
Contraindications
 Glaucoma
Precautions
 Do not increase HR greater than 100 bpm (except in paediatric patients)
 A.F.
 A.Fib.
 Bradycardia in the setting of an acute MI is common and probably beneficial. Do not treat unless
there are signs of poor perfusion (low blood pressure, confusion). Chest pain could be due to the
MI or due to poor perfusion caused by the bradycardia itself.
 IV
 IO
 IM
Side Effects
 Tachycardia
 Palpitations
 Dry mouth
 Dilated pupils and blurred vision
 Retention of urine
 Anxiety, confusion and restlessness in high doses
 Heat intolerance or impaired temperature regulation can occur in patients in hot climates
Special Notes
 Physostigmine is the antidote in the case of Atropine overdose or poisoning
 The elimination half-life of Atropine is more than doubled in children < 2 years old and the elderly
(> 65 years old)
 Onset < 2 minutes
 Peak < 5 minutes
 Duration 2-6 hours
ATROPINE DOSAGE
ADULT
BRADYCARDIA
 0.5mg IV/IO (do not administer doses less than 0.5mg IV in adults as it can produce
paradoxical bradycardia)
 Repeat every 3-5 minutes up to 3mg maximum
ORGANOPHOSPHATE POISONING
 1mg IV/IO/IM
 Repeat as required every 5 min. until secretions reduce
PAEDIATRIC
BRADYCARDIA
 0.02 mg/kg IV/IO (min dose 0.1mg, max single dose 0.5mg)
 Repeat once if required
ORGANOPHOSPHATE POISONING
 0.05mg/kg IV/IO/IM– max 2mg dose
 Repeat as required every 5 min. until secretions reduce
PAEDIATRIC ATROPINE DOSAGES
Weight Paediatric Bradycardia Organophosphate poisoning

IV/IO (0.02 mg/kg) Volume IV/IO (0.05 mg/kg) Volume
Drug concentration: 1mg/10 ml Drug concentration: 1mg/1 ml
3 kg 0.06 mg 0.6 ml 0.15 mg 0.15 ml
4 kg 0.08 mg 0.8 ml 0.2 mg 0.2 ml
5 kg 0.1 mg 1 ml 0.25 mg 0.25 ml
6 kg 0.12 mg 1.2 ml 0.3 mg 0.3 ml
7 kg 0.14 mg 1.4 ml 0.35 mg 0.35 ml
8 kg 0.16 mg 1.6 ml 0.4 mg 0.4 ml
9 kg 0.18 mg 1.8 ml 0.45 mg 0.45 ml
10 kg 0.2 mg 1 ml 0.5 mg 0.5 ml
12 kg 0.24 mg 2.4 ml 0.6 mg 0.6 ml
14 kg 0.28 mg 2.8 ml 0.7 mg 0.7 ml
16 kg 0.32 mg 3.2 ml 0.8 mg 0.8 ml
18 kg 0.36 mg 3.6 ml 0.9 mg 0.9 ml
25 kg 1 mg 1 ml
28 kg 1.4 mg 1.4 ml
31 kg 1.5 mg 1.5 ml
34 kg 0.5 mg 5 ml 1.7 mg 1.7 ml
37 kg 1.85 mg 1.85 ml
40 kg
2 mg 2 ml
43 kg
Budesonide
PHARMACOLOGY
Class
Anti-inflammatory glucocorticoid
Action
 Anti-inflammatory and immunosuppressant agent
 Reduces the body’s natural defense response
 Depresses formation, release and activity of endogenous mediators of inflammation including
prostaglandins, kinins, histamine, liposomal enzymes and complement system. It also modifies
the body’s immune response.
 Reduces symptoms associated with allergic-type reactions
 Inhibits macrophage accumulation in inflamed areas
 Reduces capillary wall permeability and oedema formation
 Antagonises histamine activity and release of kinin from substrates
 Depresses reactivity of tissues to antigen-antibody interactions
Metabolism
 Metabolised in most tissues, but primarily in the liver – to inactive compounds
 Is removed rapidly from the blood and distributed to muscle, liver, skin, intestines and kidneys
 Excreted by the kidneys
 Croup: mild, moderate and severe if unable to administer oral Dexamethasone
Contraindications
 Known hypersensitivity to Budesonide or an ingredient contained within the preparation
 Status asthmaticus, acute bronchospasm (agent is not a bronchodilator)
Precautions
 Use cautiously in patients with renal failure.
 Patients with cirrhosis show an exaggerated response to glucocorticoids
 Inhaled (Nebulizer)
Side Effects
 Diarrhea
Special Notes
 Half-life is 2-3 hours
DOSAGES
PAEDIATRICS:
 2mg Nebulized (single dose) for all paediatric age groups.
Calcium Chloride
PHARMACOLOGY
Class
Electrolyte / Mineral
Action
 Calcium is required for the initiation and maintenance of normal muscular contractions
 It is a positive inotrope
 It is required for vasoconstriction to occur in vascular smooth muscles
 It forms a key part of the blood clotting cascade
Metabolism
 Excreted solely by the kidneys
 Calcium channel and beta blocker overdoses
 Magnesium toxicity
 Suspected hyperkalemia resulting in clinically significant bradycardia or cardiac arrest
Contraindications
 Not for routine use in cardiac arrest
 The administration of calcium salts is contraindicated where hypercalcaemia, hypercalcuria or
severe renal disease are present.
 Due to the increased risk of arrhythmias, intravenous calcium administration is contraindicated in
patients with ventricular fibrillation.
Precautions
 May cause tissue irritation if leaked into the tissues – run through free flowing IV line only
 Rapid administration may cause bradycardia or asystole. Infuse through a small IV cannula over
10 minutes to avoid irritation of the veins and high doses reaching the heart causing syncope
 The administration of calcium preparations is also contraindicated in digitalised patients (see
Interaction with Other Medicines).
Side Effects
 Tissue necrosis (if infused into tissues)
 Thrombophlebitis
 Vasospasm (coronary and cerebral)
Special Notes
Too rapid injection of calcium chloride may cause the patient to experience hot flushes, chalky taste,
peripheral vasodilation, a decrease in blood pressure and abnormal heart activity (bradycardia, ar-
rhythmia, syncope).
Onset
 Rapid
CALCIUM CHLORIDE DOSAGE
ADULT
 1g in 10ml given slowly
 Repeat if required
Clopidogrel
PHARMACOLOGY
Class
Platelet aggregation inhibitor
Action
 Clopidogrel interferes with ADP binding to its platelet receptor, and the subsequent ADP-medi-
ated activation of the GPllb / llla complex, causing an irreversible, non-competitive inhibition of
platelet aggregation, without influencing cyclo-oxygenase.
 Clopidogrel also inhibits platelet aggregation induced by other agonists by blocking amplification
of platelet activation by released ADP
Metabolism
 Metabolised by the liver into inactive and active metabolites
 Inactive metabolites excreted via urine and faeces
 Active metabolites irreversibly bind to platelets and are removed by platelet degradation process
 Chest pain of cardiac origin – STEMI and NSTEMI
 Primary anti-platelet agent in patients with true aspirin allergy
Contraindications
 Known hypersensitivity
 Active haemorrhage from
 gastric ulcers,
 intracranial haemorrhage.
 Safety in children and pregnancy not established.
Precautions
 Patients with increased bleeding risk.
 Liver impairment
 Oral
Side Effects
 Haemorrhagic disorders and bleeding tendencies
 Thrombotic thrombocytopenic purpura (TTP)
 Gastro-intestinal disturbances – abdominal pain, dyspepsia, gastritis,
 Constipation
 Skin rash and pruritis
Special Notes
 Onset approximately 30 minutes
 Duration 5 -7 days
CLOPIDOGREL DOSAGE
ADULT
 300 mg orally
Dexamethasone
PHARMACOLOGY
Class
Anti-inflammatory glucocorticoid secreted by the adrenal cortex.
Action
prostaglandins, kinins, histamine, liposomal enzymes and complement system. It also modifies
the body’s immune response.
Metabolism
 Croup: mild, moderate and severe
Contraindications
 Known hypersensitivity to dexamethasone or an ingredient contained within the preparation
 Systemic fungal infections
Precautions
 Patients with cirrhosis show an exaggerated response to glucocorticoid
 Oral
Side Effects
 Convulsions
 Cardiac arrhythmias/ ECG changes
 Hypertension
 CHF
Special Notes
 Half-life is 1.5-3.5 hours
DOSAGES
PAEDIATRICS:
 0.6 mg/kg Orally (single dose). (IV solution can be given orally)
PAEDIATRIC DEXAMETHASONE DOSAGES

Undiluted: 8mg/2ml
Age Weight Dose Volume
Term 3 - 4kg 2mg 0.5ml

3 - 7 months 5 - 7kg 4mg 1ml
8 - 12 months 8 - 11kg 6mg 1.5ml
2 - 3 years 12 - 15kg 8mg 2ml
4 - 5 years 16 - 21kg 10mg 2.5ml
6 - 7 years 22 - 28kg 12mg 3ml
Dextrose (oral & IV)
PHARMACOLOGY
Class
Carbohydrate
Composition
Dextrose 10% and water
Action
 Elevates blood glucose levels
 Metabolism
 Dextrose
 Broken down in most tissues
 Stored in the liver and muscle as glycogen
 Water
 Distributed throughout the total body water
 Oral glucose: Hypoglycaemia (RBS < 4 mmol/L) in a patient with adequate state of conscious to
take orally
 IV: Hypoglycaemia (RBS<4mmol/L and symptomatic – decreased level of consciousness)
 For the dilution and administration of certain drugs
Contraindications
 Oral glucose is contraindicated in patients who do not have airway control and are at risk of aspi-
ration
 Nil of significance for IV
Precautions
Hyperglycaemia
 oral
 I.V.
Side Effects
 Nil of significance (D5W)
 Mild venous/ local irritation (D10W)
 Tissue necrosis (D50W)
Special Notes
Oral glucose
 Onset 2-4 minutes
 Peak 5 minutes
 Duration 20 minutes
IV dextrose
 Onset 1 minute
 Half-life – approx 20-40 mins (D5W)
 Oral carbohydrates should be taken once the patient is conscious enough to eat a substantial
amount to stop the patient’s RBS reducing again
DEXTROSE DOSAGE
ADULT
 15g tube of glucose orally
 Dextrose 10%, 15 - 20g (150 - 200ml) IV/IO
 Repeat if patient still hypoglycaemic
PAEDIATRIC
 15g tube of glucose orally
 Dextrose 10%, 5 ml/kg IV/IO
 Repeat if patient still hypoglycaemic
PAEDIATRIC DEXTROSE 10% DOSAGES
Weight (in kg) Newborn 2 ml/kg

Infant/ Child 5ml/kg
3 6 ml
4 20 ml
5 25 ml
6 30 ml
7 35 ml
8 40 ml
9 45 ml
10 50 ml
12 60 ml
14 70 ml
16 80 ml
18 90 ml
25 125 ml
28 140 ml
31 155 ml
34 170 ml
37 185 ml
40 200 ml
43 215 ml
Diclofenac
PHARMACOLOGY
Class
Non-steroidal anti-inflammatory (NSAID)
Action
 Anti-inflammatory, analgesic and antipyretic properties
 Prostaglandin synthetase inhibition
Metabolism
 Metabolised in the liver
 Metabolites are excreted in bile and in the urine
 Suspected Renal colic
 Mechanical back pain
Contraindications
 History of allergy to NSAIDS or Aspirin (especially asthma symptoms)
 Do not use in patients with recent AMI, stoke or bypass surgery (< 3 months)
 Active GI ulcers
 Use of NSAIDs in patients with hypovolaemia (dehydration, bleeding) may result in acute renal
failure
 Patients using other anti-coagulant medications
 More than 6 months pregnant
 Peripheral arterial disease
 Patients on Selective Serotonin Uptake Inhibitor antidepressants
Precautions
 Use with caution in patients with history of asthma
 Long term use may lead cardiovascular side effects such as AMI or stroke
 Long term use may lead to GI bleeding (gastric ulcers)
 Skin disorders, such as dermatitis, may occur (rare)
 May precipitate allergic reaction
 Use with caution in patients with chronic hepatic or renal disorders
IM (deep IM into buttocks)
Side Effects
 GI problems (diarrhoea, flatulence, indigestion, loss of appetite, nausea)
 Headaches and dizziness
 Pain at injection site, can cause necrosis or hardening of the skin
 Vertigo
Special Notes
 Onset: 15 to 30 minutes
 Administration of Diclofenac must be deep IM into the lateral upper Gluteus Maximus muscle
(buttock) to avoid damage to the sciatic nerve
 Do not give IV bolus.
 Do not give to children or adolescents
DICLOFENAC DOSAGE
ADULTS ONLY
 (18yrs or older), 75mg deep IM, single dose only
Diphenhydramine
PHARMACOLOGY
Class
Antihistamine and anti-cholinergic
Action
 Blocks histamine receptors at H1 receptor sites (diminishes allergy symptoms)
 Blocks acetylcholine receptors (drying effects on the body)
Metabolism
 Excreted by the kidneys (a portion in its unchanged form)
 Anaphylaxis
 Allergic reaction
Contraindications
 Known hypersensitivity to Diphenhydramine or its constituents
 Asthmatic episode unrelated to allergic type reaction
 Patients taking MAOI therapy
 Past history of COPD, Bronciectasis or obstructive sleep apnoea
Precautions
 Hypotension – the drug is known to cause hypotension
 Elderly – they may be more sensitive to its side effects of dizziness, drowsiness or hypotension
 Children – are often sensitive to antihistamine effects – they may become hyperactive
 Pregnancy – ensure benefit outweighs the risk
 If the patient is concurrently taking any medication that has the potential to cause drowsiness
(CNS depressant), be aware the effect may be potentiated by the administration of Diphenhydr-
amine
 Can thicken bronchial secretions – use with caution in the patient with chronic lung disease – e.g.
bronchial asthma or chronic bronchitis
 Use with caution in patients with cirrhosis or other liver diseases
Side Effects
 Hypotension and reflex tachycardia
 Bradycardia
 Sedation and drowsiness
 Paradoxical excitation in children
 Dries bronchial secretions
 Blurred vision
 Headache
 Palpitations
Special Notes
 Will cause tissue necrosis is administered incorrectly (eg. extravasation during IV administration
or SC administration)
 Slow IV push, IO (diluted), deep IM injection only
 To be used as an adjunct therapy to adrenaline/ epinephrine when treating a patient in anaphy-
laxis
 In the overdose situation can cause cardiac arrest
 Onset: rapid
DIPHENHYDRAMINE DOSAGE
ADULT
ANAPHYLAXIS / ALLERGIC REACTION
 Diphenhydramine 50 mg IV/IO/IM
PAEDIATRIC
ANAPHYLAXIS / ALLERGIC REACTION
 Diphenhydramine 1 mg/kg (max dose 50mg) IV/IO/IM
PAEDIATRIC DIPHENHYDRAMINE DOSAGES
50 mg/ml
Weight (in kg.) IV/IO/IM (1 mg/kg) Volume
Anaphylaxis
3 3 mg
4 4 mg 0.1 ml
5 5 mg
6 6 mg
0.15 ml
7 7 mg
8 8 mg
9 9 mg 0.2 ml
10 10 mg
12 12 mg 0.25 ml
14 14 mg
0.3 ml
16 16 mg
18 18 mg 0.4 ml
25 25 mg 0.5 ml
28 28 mg 0.6 ml
31 31 mg 0.6 ml
34 34 mg 0.7 ml
37 37 mg 0.7 ml
40 40 mg 0.8 ml
43 43 mg 0.9 ml
Fentanyl
PHARMACOLOGY
Class
 Synthetic narcotic analgesic
 Opiate agonist that stimulates opiate receptors in the CNS
Actions
 Potent, short acting and rapid onset
 Central nervous system effects
 Depression – leading to analgesia
 Respiratory depression – leading to apnoea
 Dependence/ addiction
 Cardiovascular effects
 Decreases the conduction velocity through the A.V. node
 Peripheral vasodilation
Metabolism
 Metabolised by the liver and the intestinal mucosa to an inactive metabolite
 Excreted by the kidneys and in the faeces
 Severe pain
 RSI and Sedation post intubation
Contraindications
 Late second stage labour
Precautions
 Elderly patients may be more sensitive to the effects
 Patients with impaired hepatic or renal function – may have impaired clearance of the drug with
prolonged duration of action
 Current asthma
 Respiratory depression
 Patients on MAO Inhibitors
 Known addiction to narcotics
 Patients on Amiodarone can experience bradycardia, sinus arrest and hypotension
 Can have a potentiating effect when administered concurrently with other CNS depressants
 Hypotension
 IV
 IO
Side Effects
 Altered conscious state
 Dizziness
 Respiratory depression and apnoea (these effects may persist longer than the analgesic effects)
 Hypotension
 Bradycardia
 Rigidity of the diaphragm and intercostal muscles
 Rash (8% of all patients)
Special Notes
 Onset: 1 minute
 Peak: 7 - 8 minutes
 Duration: 1 - 2 hours
 Respiratory depression can be reversed with Naloxone. Be aware the Naloxone will also reverse
the analgesic effects
 In the obese patient, use “ideal body weight” not actual body weight to calculate Fentanyl dos-
ages to avoid excessive dosages in this cohort of patients. Fentanyl is a lipophylic drug, and can
have profound effects in these patients. In RSI use ideal body weight to calculate dosage.
FENTANYL DOSAGE
ADULT
PAIN MANAGEMENT
 20 mcg aliquots IV/IO, repeated 1-2 minutes apart until pain relieved or maximum of
200mcg dose)
RSI
 1 or 3 mcg/kg IV/IO as part of induction (dose based on stable/unstable patient)
DELAYED SEQUENCE INDUCTION

 100mcg IV as second dose (if required following 25mg Ketamine)
PAEDIATRIC
PAIN MANAGEMENT
 1 mcg/kg IV/IO (max 2mcg/kg)
 2 mcg/kg IN
PAEDIATRIC FENTANYL DOSAGES
Analgesia
IV/IO (1 mcg/kg) Volume IN (2 mcg/kg) Volume
Undiluted concentration –
Weight Dilute: 100 mcg (2ml) + 8 ml only dilute if necessary for
= 10 mcg/ml atomization. Max 0.3 – 0.5
ml per nostril
3 kg 3 mcg 0.3 ml 6 mcg 0.1 ml
4 kg 4 mcg 0.4 ml 8 mcg
5 kg 5 mcg 0.5 ml 10 mcg 0.2 ml
0.3 ml
0.4 ml
10 kg 10 mcg 1 ml 20 mcg
12 kg 12 mcg 1.2 ml 24 mcg 0.5 ml
14 kg 14 mcg 1.4 ml 28 mcg
0.6 ml
16 kg 16 mcg 1.6 ml 32 mcg
18 kg 18 mcg 1.8 ml 36 mcg 0.7 ml
25 kg 25 mcg 2.5 ml 50 mcg 1 ml
28 kg 28 mcg 2.8 ml 56 mcg 1.1 ml
31 kg 31 mcg 3.1 ml 62 mcg 1.2 ml
34 kg 34 mcg 3.4 ml 68 mcg 1.4 ml
37 kg 37 mcg 3.7 ml 74 mcg 1.5 ml
40 kg 40 mcg 4 ml 80 mcg 1.6 ml
43 kg 43 mcg 4.3 ml 86 mcg 1.7 ml
Furosemide
PHARMACOLOGY
Class
Loop diuretic
Action
 Causes venous dilation and reduces venous return
 Causes diuresis through inhibiting the absorption of sodium and chloride in the proximal and
distal tubules, and in the loop of Henle.
Metabolism
Excreted by the kidneys (predominantly in its unchanged form)

Acute pulmonary oedema with signs of systemic fluid overload secondary to:
 Left ventricular failure (congestive heart failure)
 Cirrhosis of the liver
 Renal disease, including nephritic syndrome
Contraindications
 Previous sensitivity to Furosemide
 Anuric patients
 Precautions
 Hypotension
 Elderly patient should be given a lower dose initially
 Patients taking Lithium should not be given Furosemide as it reduces the clearance of Lithium
and may cause Lithium toxicity
 Extreme hypotension may be seen in patients on ACE inhibitors or ARB (angiotensin receptor
blockers) – due to the potentiation of effects. Can result in renal failure.
IV
Side Effects
 Hypotension
 Anaphylactic reactions
 Tinnitus and hearing loss
 Hyperglycaemia
Special Notes
Furosemide may potentiate the effects of Succinylcholine – (a concern in the cardiac failure patient
who requires intubation)
DOSAGE
ADULT
 0.5mg/kg IV and should not exceed 40mg. Single dose only.
GLUCAGON
PHARMACOLOGY
Class
Hyperglycaemic agent
Action
 A biosynthetic form of glucagon (pancreatic hormone) which releases glucose from the liver by means of
glycogenolysis, thereby increasing blood glucose levels.
Metabolism
 Symptomatic hypoglycaemia
 ONLY if unable to obtain IV access or dextrose is unavailable or not effective.
Contraindications
 Known hypersensitivity to Glucagon
 Allergy to beef or porcine protein
 Phaeochromocytoma
Precautions
 Glucagon for hypoglycaemia is not effective in patients with marked depletion of liver glycogen stores, as in
starvation, adrenal insufficiency, or chronic hypoglycaemia.
 Insulinoma
 Ischemic heart disease
 IM
Side Effects
 Nausea and Vomiting – dose related
 Dizziness, light-headedness, skin rash, dyspnea (all uncommon)
 Hypokalaemia
 Myocardial ischemia may be aggravated in patients with pre-existing cardiac disease
Special Notes
 The effects of Glucagon wear off rapidly. Oral glucose should be provided to the patient once the patient has
regained consciousness. Monitor for secondary hypoglycaemia.
 Provide IV dextrose as soon as possible
DOSAGES
ADULTS:
 1mg IM
PAEDIATRICS (CCP only):

 <20kg (<6years): 0.5mg IM
 >20kg : 1mg IM
 Not for neonates.
Glyceryl Trinitrate – GTN
(sublingual and IV)
PHARMACOLOGY
Class
 A nitrate
 Principally a vascular smooth muscle relaxant
Actions
 Glyceryl Trinitrate forms the free radical nitrous oxide (NO) – which is a potent smooth
muscle relaxant, resulting in vasodilation
 Venous dilation promotes venous pooling and reduces venous return to the heart
 Reduces preload
 Arterial dilation reduces systemic vascular resistance and arterial pressure
 Reduces afterload
 The reduction in preload and afterload results in;
 Reduced myocardial oxygen demand
 Reduced systolic, diastolic and mean arterial pressure – whilst usually maintaining coronary per-
fusion pressure
 Mild collateral coronary artery dilation improves blood supply to ischaemic areas of myocardium
 Reductions in BP may result in a compensatory rise in HR (usually mild)
Metabolism
 In the liver by first pass hepatic metabolism
 Chest pain associated with suspected acute coronary syndrome
 Hypertensive Emergencies causing acute coronary syndrome and acute flash pulmonary oede-
ma
 Acute left ventricular failure with pulmonary oedema
Contraindications
 Systolic BP < 90
 Bradycardia < 50 bpm
 VT (Ventricular tachycardia)
 Use of PED5 Inhibitors. Sildenafil Citrate (“Viagra”) or Vardenafil (“Levitra”) within the previous 24
hours, or Tadalafil (“Cialis”) use within the previous 4 days.
Precautions
 Suspected right ventricular infarction
 Heart rate greater than 150
 Sublingual/ buccal
 IV Infusion
Side Effects
 Headache
 Hypotension
 Tachycardia
 Palpitations
 Bradycardia
 Dizziness
 Flushing of the skin
Special Notes
 Do not delay administration in order to obtain a 12-Lead in suspected ACS.
 Sublingual effects
 Peak: 5 minutes
 Duration: 25 minutes
 IV effects
 Duration 3-5 minutes
DOSAGE
ADULT
CHEST PAIN OF A CARDIAC NATURE
 1 spray (0.4mg) SL
 Repeat every 5 minutes if pain persists and patient’s BP remains > 100/Systolic
 If no pain relief after 3 doses use alternative analgesia
ACUTE PULMONARY OEDEMA:
 Normal to High BP – 1-3 spray S/L while preparing IV infusion, repeat 1 spray every 5
minutes until CPAP applied.
 High BP SBP>160mmHg – 3 spray S/L while preparing IV infusion, repeat 1 spray
every 5 minutes until CPAP applied.
 IV infusions for APO (Normal to High BP)
Dilution:
 If required dilute GTN to achieve final concentration of 1mg/ml

 Start at 6ml/hr (100mcg/min)
 Increase or decrease dose as required by 0.6ml/hr increments (titrate to effect)
 Monitor BP response.
Hydrocortisone
PHARMACOLOGY
Class
Anti-inflammatory glucocorticoid secreted by the adrenal cortex.
Action
prostaglandins, kinins, histamine, liposomal enzymes and complement system. It a283lso
modifies the body’s immune response.
Metabolism
 For control of severe or incapacitating allergic conditions intractable to other treatments and for
the control of acute manifestations, including anaphylactic and anaphylactoid reactions.
 Asthmatic patient – as an adjunct for moderate to severe exacerbations of asthma, (speeds the
resolution of airflow obstruction and reduces the rate of relapse). To be administered if the re-
sponse to oral inhalation therapy is not immediate or sustained.
 Exacerbation of COPD (NB: the effects are much less dramatic than in asthma)
Contraindications
 Known hypersensitivity to hydrocortisone or an ingredient contained within the preparation
 Systemic fungal infections
 IM administration for conditions prone to bleeding (eg. idiopathic thrombocytopenic purpura (ITP)
Precautions
 Patients with cirrhosis show an exaggerated response to glucocorticoids
 Elderly may require lower doses.
 Use with caution in recent MI patients as there is an association with glucocorticoid use and Left
ventricular free-wall rupture
 Slow IV administration (over a period of not less than 30 seconds)
 IM administration
Side Effects
 Convulsions
 Cardiac arrhythmias/ ECG changes
 Hypertension
 CHF
Special Notes
 Half-life is 1.5-3.5 hours
DOSAGES
ADULTS
 anaphylaxis and bronchoconstriction: 200mg IV
PAEDIATRICS:
 5mg/kg IV up to maximum of 200mg
PAEDIATRIC HYDROCORTISONE DOSAGES
Reconstituted – 100 mg / 2 ml
Weight
Asthma and Anaphylaxis
3 kg 15 mg 0.3 ml
4 kg 20 mg 0.4 ml
5 kg 25 mg 0.5 ml
6 kg 30 mg 0.6 ml
7 kg 35 mg 0.7 ml
8 kg 40 mg 0.8 ml
9 kg 45 mg 0.9 ml
10 kg 50 mg 1 ml
12 kg 60 mg 1.2 ml
14 kg 70 mg 1.4 ml
16 kg 80 mg 1.6 ml
18 kg 90 mg 1.8 ml
25 kg 125 mg 2.5 ml
28 kg 140 mg 2.8 ml
31 kg 155 mg 3.1 ml
34 kg 170 mg 3.4 ml
37 kg 185 mg 3.7 ml
40 kg 200 mg 4 ml
43 kg 200 mg 4 ml
Ibuprofen
PHARMACOLOGY
Class
NSAIDS – Non steroidal anti-inflammatory drugs
Action
 Block the enzyme which produces prostaglandins (cyclo-oxygenase) – resulting in lower levels of
prostaglandins – thus causing a reduction in inflammation, pain and fever.
 Reduces the ability of the blood to clot
Metabolism
 Is primarily metabolized in the liver
 The inactive metabolite is excreted in the urine
 Management of mild to moderate pain
 To reduce fever
 As an anti-inflammatory
Contraindications
 Pregnancy
 Allergies to other NSAIDS (eg: aspirin)
 Asthmatic patients – more likely to experience allergic reactions
 In patients less than 6 weeks following an AMI – increased risk of cardiac free wall rupture and
death.
Precautions
Use with caution in patients with dehydration, impaired kidney function or congestive heart failure –
because NSAIDs reduce the flow of blood to the kidneys and impair function of the kidneys.
Oral
Side Effects
 Rash
 Tinnitus (ringing in the ears)
 Headaches
 Dizziness
 Abdominal pain, nausea and diarrhoea
 Heartburn
 Gastrointestinal bleeding
Special Notes
 Maximum dose is 1.2g daily
 Should be taken with food to prevent stomach issues
 Not recommended during pregnancy
 Safe to use while breastfeeding
DOSAGE
ADULTS
 200 - 400mg orally every 4 - 6 hours
Ipratropium bromide
PHARMACOLOGY
Class
Anti-cholinergic bronchodilator (chemically related to Atropine)
Action
 Parasympathetic agent
 Inhibits vagal reflexes by antagonising the action of ACh, the transmitter agent released from the
vagus nerve.
 Has a synergistic effect with Beta 2 agonists to mediate bronchoconstriction.
Metabolism
 It is only partially metabolised.
 More than half is excreted by the kidneys unchanged.
Moderate or severe respiratory distress associated with bronchospasm, in patients with asthma, and
chronic obstructive pulmonary disease (including chronic bronchitis and emphysema).
Contraindications
 Known hypersensitivity to Ipratropium Bromide
 Known hypersensitivity to Atropine or its derivatives
Precautions
Avoid contact with the eyes
Nebulised in conjunction with Salbutamol
Side Effects
 Headache
 Nausea
 Dry mouth
 Skin rash
 Tachycardia (rare)
 Palpitations (rare)
 Allergic reactions or anaphylaxis
 Worsening of narrow angled glaucoma (especially if solution comes into contact with the eyes)
Special Notes
 Onset: 5 minutes
 Protect ampoules from light
DOSAGE
ADULTS:
 0.5mg nebulised with Salbutamol over 10 minutes. If repeat dose is necessary CCP
must be requested and administration should be en route to hospital.
PAEDIATRICS:
 Infants and children < 6 years old 0.25mg Atrovent + 2.5mg Salbutamol rebulised
 Children > 6 years old 0.25 - 0.5mg Atrovent + 2.5mg - 5mg Salbutamol rebulised over
10 minutes
 If repeat dose is necessary CCP must be requested and administration should be en
route to hospital.
Ketamine
PHARMACOLOGY
Class
Dissociative anaesthetic (non-barbiturate)
Action
 Dissociates higher cortical function from the brain stem
 Analgesic
 Does not impair pharyngeal or laryngeal reflexes
Metabolism
 Rapidly distributed to other tissues
 Excreted by the kidneys (85-95%)
 Minimal amounts excreted in the bile and faeces
 Rapid Sequence Induction
 Procedural Sedation
 Sedation of the combative patient
 Analgesia
 severe pain secondary to trauma refractory to opioid analgesia.
 In situations where there is concern regarding airway maintenance (eg. entrapment)
 Conscious sedation in adult and paediatrics
Contraindications
 Any patient where a significant elevation in BP would constitute a serious hazard
 Paediatric patients < 3 months old
 Cardiac patients where an increase in BP or HR would be detrimental to their condition
Precautions
 Elderly patients – use a half dose (elderly patients usually have some level of decreased hepatic,
renal or cardiac function)
 Consider a half dose if the patient has already received narcotic analgesia or is taking barbitu-
rates
 Chronic alcoholics or acutely-intoxicated patient
 IV / IO
 IM
Side Effects
 Hypersensitivity reaction/ allergic reaction
 Increase in HR and/or BP
 Increased bronchial secretions and Hypersalivation – especially in paediatric patients
 Emergence reaction (dysphoria) as the drug wears off (reduce stimulation to minimise this effect)
 Laryngospasm
 Respiratory stimulation or severe respiratory depression – including apnoea (respiratory depres-
sive effects are often seen after rapid IV administration)
Special Notes
 Administration of the dose should occur over a 60-second period to reduce respiratory and pres-
sor responses.
 Onset: rapid
 Peak: 10 - 15 minutes
DOSAGE
ADULTS
ANALGESIA
 0.25 - 0.5 mg/kg IV/IO (Repeat as required)
 0.5 - 1mg/kg IM/IN (Repeat every 5-10 minutes as required)
CONSCIOUS/ PROCEDURAL SEDATION:

 Light sedation: 0.5mg/kg IV/IO or 1 - 2mg/kg IN/IM
 Deeper sedation: 1-1.5mg/kg IV/IO or 3 - 4mg/kg IN/IM
RSI
 Induction dose 1 to 2 mg/kg IV/IO (dose based on stable/ unstable patient)
DELAYED SEQUENCE INTUBATION
 25mg IV (repeat if required)
 Post-RSI sedation (adults and paediatrics) 0.5 mg/kg IV at 15 - 20 minute intervals
as required.
PAEDIATRIC
ANALGESIA
 0.25 - 0.5 mg/kg IV/IO (Repeat as required)
 0.5 - 1mg/kg IM/IN (Repeat every 5-10 minutes as required)
CONSCIOUS/PROCEDURAL SEDATION:
 Light sedation: 0.5mg/kg IV/IO or 1 - 2mg/kg IN/IM
 Deeper sedation: 1-1.5mg/kg IV/IO or 2 - 4mg/kg IN/IM
PAEDIATRIC KETAMINE DOSAGES
Weight IV/IO Volume IV/IO (0.5 Volume IN/IM Volume IN/IM Vol-
(0.25 mg/ mg/kg) (1.0 mg/ (2.0 ume
kg) kg) mg/kg)
Dilute to 25mg/ml – 500 mg (10 ml) + 10 ml NaCl Undiluted concentration – only dilute if nec-
essary for atomization. Max 0.3 – 0.5 ml per
nostril
Analgesia and procedural sedation
10 kg 2.5 mg 0.1 ml 5 mg 0.2 ml 10 mg 0.2 ml 20mg 0.4ml
12 kg 3 mg 0.12 ml 6 mg 0.24 ml 12 mg 24mg 0.48ml
16 kg 4 mg 0.16 ml 8 mg 0.32 ml 16 mg 0.32 ml 32mg 0.64ml
25 kg 6.25 mg 0.25 ml 12.5 mg 0.5 ml 25 mg 0.5 ml 50mg 1ml
31 kg 7.75 mg 0.31 ml 15.5 mg 0.62 ml 31 mg 0.62 ml 62mg 1.2ml
37 kg 9.25 mg 0.37 ml 18.5 mg 0.74 ml 37 mg 0.74 ml 74mg 1.5ml
Keterolac
PHARMACOLOGY
Class
 Non-steroidal anti-inflammatory (NSAID)
Action
 Anti-inflammatory, analgesic and antipyretic properties
 Prostaglandin synthetase inhibition
Metabolism
 Metabolites are excreted in bile and in the urine
 ADULT PATIENTS ONLY
 Suspected renal colic
 Mechanical back pain and/ or muscular skeletal pain
 CCP ONLY for Migraine
Contraindications
 Age under 18 years
 History of allergy to NSAIDS or Aspirin (especially asthma symptoms)
 Severe heart failure, hepatic failure and renal failure
 Do not administer if patient has received an NSAID within the previous 6 hours (e.g. ibuprofen)
 Do not use in patients with recent AMI, stoke or bypass surgery (<3 months)
 Active GI ulcers
 Do not use if you suspect activing bleeding (excluding menstruation) or that the patient is clinical-
ly dehydrated.
 Patients using other anti-coagulant medications
 More than 6 months pregnant
 Peripheral arterial disease
 Patients on Selective Serotonin Uptake Inhibitor antidepressants.
Precautions
 Use with caution in patients with history of asthma
 Use with caution in the elderly (over 75) or patients with low body weight (less than 50kg based
on estimated weight)
 Use with caution in patients receiving long-term NSAID therapy
 Use with caution in patients who may be fluid depleted (but not clinically dehydrated) IF required
administer 500ml fluid bolus (fluid bolus is recommended in patients who have been working
outdoors or under rigorous conditions)
 Long term use may lead to cardiovascular side effects such as AMI or stroke
 Long term use may lead to GI bleeding (gastric ulcers)
 Skin disorders, such as dermatitis, may occur (rare)
 May precipitate allergic reaction
 Use with caution in patients with chronic hepatic or renal disorders
 Via the intravenous or intramuscular route
Presentation
 Ketorolac is presented as 30mg/1ml solution
Route of Administration – Intravenous administration
 Draw up ALL 30mg/1ml of drug into a 3ml syringe.
 Dilute with 2ml 0.9% Saline to a total of 3ml.
 Discard 2ml (20mg of drug) leaving 1ml (10mg) for intravenous injection.
 Administer 1ml (10mg) as a slow intravenous bolus over 10 seconds.
Route of Administration – Intramuscular administration
 Draw up ALL 30mg/1ml of drug into a 1ml syringe.
 Discard 0.7ml and administer 0.3ml intramuscularly.
Side Effects
 GI problems (diarrhea, flatulence, indigestion, loss of appetite, nausea)
 Headaches and dizziness
 Pain at injection site, can cause necrosis or hardening of the skin
 Vertigo
Special Notes
 Onset: upwards of 30 minutes
 Appropriate monitoring and advice are required for patients with a history of hypertension and/
or mild to moderate congestive heart failure as fluid retention and oedema have been reported in
association with NSAID therapy.
 Patients with uncontrolled hypertension, congestive heart failure, established ischaemic heart
disease, peripheral arterial disease, and/or cerebrovascular disease should only be treated with
ketorolac after careful consideration.
 Do not give to children or adolescents.
 Encourage patient to take oral fluids or consider administration of 250-500ml intravenous fluid
bolus.
 Consider other analgesic medication in the elderly patients (over 75 years or age).
 Consider other analgesic medication in patients with low body weight (less than 50kg).
KETOROLAC DOSAGE
ADULTS ONLY
 (18yrs or older), 10mg IV or IM, single dose only
Magnesium sulphate
PHARMACOLOGY
Class
Electrolyte (Mg2+)
Actions
 CNS depressant
 Anti-convulsant (works to block neuromuscular transmission and decreasing the amount of ACh
liberated at the end plate by the motor nerve impulse)
 Anti-arrhythmic
 Smooth muscle relaxant (bronchial, vascular and uterine tissue)
 Effects of overdose can be antagonised by administration of IV Calcium
Metabolism
 Excreted solely by the kidneys
 Pre-eclampsia
 Eclampsia
 Torsades de pointes
 Severe asthma
Contraindications
 Shock
 Heart block/ heart failure
 Addison’s disease
 Infective hepatitis
Precautions
 Use with caution in patients with renal failure.
 Due to the Aluminium content in the preparation which can be toxic in patients with impaired
kidney function.
 Because the kidneys are the sole way of excreting the drug, any impairment in kidney function
could be detrimental.
 Myasthenia Gravis
 Patients using medications that have the potential to cause drowsiness (narcotics, anti-his-
tamines, muscle relaxants etc.) can have an increased drowsiness effect when administered
Magnesium.
 IV
 IO
 IM
Side Effects
 Drowsiness
 Respiratory depression
 Heart block
 Muscle weakness
 Dizziness
 Skin flushing and sweating
 Hypotension
Special Notes
 Magnesium comes in 10% in 20ml (0.8meq/ml) which is a total of 2g/ vial.
 Anticonvulsant action is immediate
 Lasts approximately 30 minutes
DOSAGE
ADULT
BRONCHOCONSTRICTION
2g IV over 20 minutes
TORSADES DE POINTES
 2 g (20ml) administered slowly via IV/IO administered over 10 minutes.
PRE-ECLAMPSIA AND ECLAMPSIA

 4g in 100ml 0.9% NaCl – infused over 10 minutes – IV/IO
Instruction for dilution
 Bronchospasm: 1 ampoule in a 20ml syringe. Concentration is 100mg/ml i.e. No dilution

required - run at 120ml/hr
 Eclampsia: 4g (40ml: 10% solution) – diluted in 10ml 0.9% NaCl (50ml syringe) adminis-
tered IV slowly over a period of 10 minutes - run at 300ml/hr
PAEDIATRIC
BRONCHOCONSTRICTION
 Paediatrics 25-50mg/kg IV maximum of 2g over 20 minutes
TORSADES DE POINTES
 Paediatrics 25-50mg/kg IV maximum of 2g over 20 minutes
PAEDIATRIC MAGNESIUM SULPHATE DOSAGES
Drug concentration: 100 mg/ml

Weight IV/IO (25 Volume IV/IO (50 Volume
mg/kg) mg/kg)
3 kg 75 mg 0.75 ml 150 mg 1.5 ml
4 kg 100 mg 1 ml 200 mg 2 ml
5 kg 125 mg 1.25 ml 250 mg 2.5 ml
6 kg 150 mg 1.5 ml 300 mg 3 ml
7 kg 175 mg 1.8 ml 350 mg 3.5 ml
8 kg 200 mg 2 ml 400 mg 4 ml
9 kg 225 mg 2.3 ml 450 mg 4.5 ml
10 kg 250 mg 2.5 ml 500 mg 5 ml
12 kg 300 mg 3 ml 600 mg 6 ml
14 kg 350 mg 3.5 ml 700 mg 7 ml
16 kg 400 mg 4 ml 800 mg 8 ml
18 kg 450 mg 4.5 ml 900 mg 9 ml
25 kg 625 mg 6.25 ml 1250 mg 12.5 ml
28 kg 700 mg 7 ml 1400 mg 14 ml
31 kg 775 mg 7.75 ml 1550 mg 15.5 ml
34 kg 850 mg 8.5 ml 1700 mg 17 ml
37 kg 925 mg 9.25 ml 1850 mg 18.5 ml
40 kg 1000 mg 10 ml 2000 mg 20 ml
43 kg 1000 mg 10 ml 2000 mg 20 ml
Methoxyflurane (penthrox)
PHARMACOLOGY
Class
Central nervous system depressant
Action
Inhalational analgesic at low concentrations
Metabolism
 By the liver
 Excreted by the lungs
 Pain relief
 Cardiac chest pain
 Child birth
 Obstetric pain
Contraindications
 Pre-existing renal disease/ renal impairment
 Concurrent use of Tetracycline antibiotics
 Exceeding 6mls within a 24-hour period
 Known severe adverse reaction
 Malignant hyperthermia (MH occurs when a triggering agent is given to a susceptible individual –
Methoxyflurane is a known trigger)
 Patient unable to follow instructions
Precautions
 Pre-eclampsia
 Route of Administration
 Supervised self-administration utilising the “Penthrox” inhaler
Side Effects
 Drowsiness
 Decrease in BP
 Bradycardia (rare)
 Exceeding the maximum dose of 6mls in a 24-hour period may cause renal toxicity
Special Notes
 The initial priming dose of Methoxyflurane is 3mls. This provides approximately 25 minutes of
analgesia. A second 3ml dose may be administered in the initial inhaler if required.
 Maximum 6mls in a 24-hour period
 Onset approximately 1 minute (8 breaths)
 Duration: 5-10 minutes
DOSAGE
 3mls via inhaler

 May be repeated after 25 minutes
Metoclopramide
PHARMACOLOGY
Class
Mild 5HT3 receptor antagonist
Action
 Antiemetic
 stimulates motility of the upper gastrointestinal tract without stimulating gastric, biliary or pancre-
atic secretions
 increases the tone and amplitude of gastric contraction, relaxes pyloric sphincter and increases
peristalsis of the small intestine – resulting in accelerated gastric emptying
 Dopamine antagonism within the chemoreceptor trigger zone may also contribute to the anti-
emetic activity
Metabolism
Primary Emergency Indications (If Ondansetron is not available)
For the treatment of nausea and vomiting in:
 Chest pain / discomfort of a cardiac nature
 Previously diagnosed migraine
 Severe gastroenteritis
 Eye trauma
Contraindications
 Hypersensitivity – to metoclopramide or sodium metabisulphite
 Gastrointestinal haemorrhage
 Bowel obstruction or perforation (suspected or diagnosed)
 Pheochromocytoma – it may precipitate acute hypertensive response
 Epilepsy
 In patients who have had gastrointestinal surgery within the last 3-4 days
 Children due to extra-pyramidal side effects
Precautions
 Abdominal pain of unknown etiology
 Use reduced doses in patients with hepatic impairment or severe renal impairment
 IV
 IM
 IO
Side Effects
 Anxiety
 Restlessness
 Drowsiness
 Lethargy
 Dry mouth
 Muscle tremor
 Extrapyramidial reactions (usually dystonic in nature)
 Allergic-type reactions
Special Notes
Not effective for motion sickness
DOSAGE
ADULTS ONLY
 10mg IV/IO over 1 minute
Midazolam
PHARMACOLOGY
Class
Benzodiazepine
Actions
 Short acting central nervous system depressant, with the following properties
 Anti-convulsant
 Sedative
 Hypnotic
 Amnesic agent
 Skeletal muscle relaxant
 Anxiolytic
Metabolism
 Epileptic seizures
 Sedation for cardioversion
 Sedation for TCP (transcutaneous pacing)
 Combative patients
 For anxiolysis in analgesia
 Eclamptic seizure ONLY if Magnesium is not available or not succesful in terminating active sei-
zure
Contraindications
Hypersensitivity to Benzodiazepines or any of the excipients
Precautions
 The effects may be prolonged in patients with hepatic impairment – consider using reduced dos-
es – (due to prolonged elimination and lower clearance rates)
 The effects may be prolonged in patients with renal impairment – consider using reduced doses –
(these patients are more sensitive to the sedative effects of Midazolam)
 Also consider using reduced doses in patients with:
 Severe respiratory depression
 Haemodynamic instability
 Elderly patients - > 60 years old – (the elimination half life is prolonged up to 4 times)
 Patients with decompensated heart failure
 Chronically ill patients
 Patients with Myasthenia Gravis
 Epileptic patients treated with Sodium Valproate
 Effects may be exaggerated in patients presenting with acute alcohol intoxication
 Pregnancy – the risks to the mother and foetus must be considered as there are documented
risks to foetal health (as Midazolam crosses the placenta)
 IV
 IM
 IO
 Intranasal / buccal
Side Effects
 Depressed level of consciousness
 Respiratory depression and respiratory arrest
 Laryngospasm
 Depressed myocardial contractility
 Loss of airway control
 Hypotension
Special Notes
 Paediatrics have an increased metabolic clearance of the drug
 Protect from light
 Onset: 1-3 minutes IV administration, IM up to 15 minutes.
 Duration of action: 30 minutes
 Rapid metabolic transformation
DOSAGE
ADULT
DELAYED SEQUENCE INDUCTION OF INTUBATION
 2mg IV as second dose (if required following Ketamine 25mg)
BRADYCARDIA REQUIRING TRANSCUTANEOUS PACING

 0.1mg/kg slowly IV/IO after pacing initiated and BP is stable. Maximum dose 3mg. IV
dose can be repeated up to a total of 10mg.
RAPID AF, SVT AND VT WITH A PULSE REQUIRING CARDIOVERSION
 0.1mg/kg slowly IV/IO unless severely hypotensive (BP< 90 systolic). Maximum dose
5mg. IV dose can be repeated up to a total of 20mg.
SEIZURE
 0.2mg/kg Intranasal/ buccally, with not more than 1ml per nostril per dose.
 0.2mg/kg IM up to maximum of 2ml per injection site (10mg). IM dose may be repeat-
ed after 15 minutes if required.
 0.1mg/kg IV/IO (ideal body weight)
 Dose may be repeated up to 0.2mg/kg after 5 minutes if required. Aliquots (Incremental
doses) of 5mg/dose for the IV/IO route can be repeated up to a total of 20mg.
ANALGESIA (PAIN WITH ASSOCIATED SEVERE ANXIETY)

 Up to 3mg in combination with analgesic
SEDATION FOR COMBATIVE PATIENTS

 0.1mg/kg IM (with maximum single dose of 10mg).
PAEDIATRIC
SEIZURE
0.2 mg/kg buccally / nasally / IM or
0.1mg/kg IV/IO in 5mg increments, maximum dose 10mg.
IV dose may be repeated after 5 minutes, IM dose after 15 minutes if required.
PAEDIATRIC MIDAZOLAM DOSAGES
Seizures
IV/IO/IM (0.1 IN/buccal
Volume Volume
mg/kg) (0.2 mg/kg)
Weight Undiluted concentration –

Dilute to 1mg/ml 15mg (3 ml) only dilute if necessary for
+ 12 ml NaCl atomization. Max 0.3 – 0.5 ml
per nostril
3 kg 0.3 mg 0.3 ml 0.6 mg 0.1 ml
4 kg 0.4 mg 0.4 ml 0.8 mg
5 kg 0.5 mg 0.5 ml 1 mg 0.2 ml
6 kg 0.6 mg 0.6 ml 1.2 mg
7 kg 0.7 mg 0.7 ml 1.4 mg
0.3 ml
8 kg 0.8 mg 0.8 ml 1.6 mg
9 kg 0.9 mg 0.9 ml 1.8 mg
0.4 ml
10 kg 1 mg 1 ml 2 mg
12 kg 1.2 mg 1.2 ml 2.4 mg 0.5 ml
14 kg 1.4 mg 1.4 ml 2.8 mg
0.6 ml
16 kg 1.6 mg 1.6 ml 3.2 mg
18 kg 1.8 mg 1.8 ml 3.6 mg 0.7 ml
25 kg 2.5 mg 2.5 ml 5 mg 1 ml
28 kg 2.8 mg 2.8 ml 5.6 mg 1.1 ml
31 kg 3.1 mg 3.1 ml 6.2 mg 1.2 ml
34 kg 3.4 mg 3.4 ml 6.8 mg 1.4 ml
37 kg 3.7 mg 3.7 ml 7.4 mg 1.5 ml
40 kg 4 mg 4 ml 8 mg 1.6 ml
43 kg 4.3 mg 4.3 ml 8.6 mg 1.7 ml
Naloxone
PHARMACOLOGY
Class
Narcotic antagonist/ opioid antagonist
Action
 Prevents or reverses the effects of narcotics by blocking the opioid receptors and competing with
opioids for the receptor sites.
 It is a “pure” opioid antagonist – and does not cause side effects when no opioids are present.
Metabolism
Metabolised by the liver

Actual or suspected opioid overdose
Contraindications
 Patient with a traumatic head injury
Precautions
 If administered to patients who are known to be dependent on narcotics it can precipitate sudden
withdrawal syndrome
 Neonates
 IM/ IN
 IV/ IO
 SC
Side Effects
 In the patient with no narcotics in their system;
 In patients with narcotics in their system;
 Signs and symptoms associated with abrupt reversal of opioids – “acute withdrawal syndrome”
 Sweating
 Tachycardia
 Hypertension
 Seizures
 VT or VF
 APO
 Cardiac arrest and death
 Agitation
 Tremors
 Dilated pupils
Special Notes
 The duration of action of Naloxone is often less than that of the narcotic administered. Therefore,
repeated doses may be required.
 If the mother of a neonate has received narcotics within 1 hour prior to delivery the neonate may
have narcotic related respiratory depression.
 Onset 2 minutes
 Duration: approx 45 minutes
 Half life: 60 minutes
DOSAGE
ADULT
NARCOTIC OVERDOSE
 To reverse the overdose 0.4 - 2mg (IV/IM/IO) repeated every 2 - 3 minutes up to 10mg.
 IN route: 2mg of IV solution via nasal atomizer
 To only reverse the respiratory depression, administer 100mcg bolus as
necessary until desired respiratory rate recovery.
PAEDIATRIC
NARCOTIC OVERDOSE
 0.01mg/kg IV/IM/IO – maximum single dose 0.4mg. IV dose can be repeated every 2
minutes up to 4 times (5 doses in total). IM/SC dose can be repeated every 15 min-
utes up to 4 times (5 doses in total). Maximum total dose of 2mg.
PAEDIATRIC NALOXONE DOSAGES
Narcotic overdose
IV/IO/IM (0.01 mg/
Volume
kg)
Weight
Dilute: 0.4mg (1 ml) + 3ml (NaCl) =
0.1 mg/ml
3 kg 0.03 mg 0.3 ml
4 kg 0.04 mg 0.4 ml
5 kg 0.05 mg 0.5 ml
6 kg 0.06 mg 0.6 ml
7 kg 0.07 mg 0.7 ml
8 kg 0.08 mg 0.8 ml
9 kg 0.09 mg 0.9 ml
10 kg 0.1 mg 1 ml
12 kg 0.12 mg 1.2 ml
14 kg 0.14 mg 1.4 ml
16 kg 0.16 mg 1.6 ml
18 kg 0.18 mg 1.8 ml
25 kg 0.25 mg 2.5 ml
28 kg 0.28 mg 2.8 ml
31 kg 0.31 mg 3.1 ml
34 kg 0.34 mg 3.4 ml
37 kg 0.37 mg 3.7 ml
40 kg 0.4 mg 4 ml
43 kg 0.4 mg 4 ml
Noradrenaline
PHARMACOLOGY
Class
Sympathomimetic
Action
 Direct action on alpha receptors (potent)
 Direct effect on beta-1 receptors (moderate to weak)
Metabolism
 Methylation by catechol-o-methyltransferase
 Deamination by manoamine oxydase (MAO)
 Ultimate metabolites from both is 4- hydroxy-3-methoxymandelic acid
 Management of symptomatic drug induced hypotension
 Management of symptomatic hypotension in patients with septic shock
 Management of symptomatic hypotension in the major trauma patient unresponsive to fluid therapy in
order to maintain cerebral perfusion.
 Management of Cardiogenic shock.
 Management of Neurogenic shock.
Contraindications
Known hypersensitivity to noradrenaline
Precautions
 Dilute in 5% dextrose or isotonic dextrose saline
 Use by syringe driver only
 Administration through peripheral IV only in emergency setting. Ensure IV line is correctly placed and free
flowing.
 IV, (central line is the preferred route. Peripheral IV only in the emergency setting)
 IO
Side Effects
 severe peripheral and visceral vasoconstriction resulting in arterial hypotension
 decrease in renal blood flow
 decrease in urine production
Special Notes
 Onset rapid
 Peak
 Duration 1 - 2 minutes
 NB: If administering emergency infusion through peripheral IV, ensure that IV is well placed and flowing freely
(Forearm is preferred site). 18G or larger is preferred size cannula. Monitor closely for extravasation. If
extravasation occurs, stop infusion immediately and disconnect. Gently aspirate extravasated solution (Do
NOT flush the line); remove needle/cannula; elevate extremity. Report extravasation to ED staff on handover.
DOSAGE
SEPTIC SHOCK, CARDIOGENIC SHOCK & SHOCK WITH HYPOTENSION

REFRACTORY TO FLUID RESUSCITATION (Trauma unresponsive to fluids)
 Continuous infusion titrated to blood pressure/MAP target
 Draw 1 amp of Noradrenaline 4mg (1 x amp 4mg/4ml) into 50 ml syringe and dilute
with 46ml NaCl = 4mg/50ml (80mcg/ml)
 Using a syringe driver, start the infusion at 0.01mcg/kg/minute. Increase rate by
0.05mcg/kg/min if required to achieve desired effect.
INTERFACILITY TRANSFERS
 Follow MICU prescribed dilution and dosing per patient
 Continuous infusion titrated to blood pressure target
Ondansetron
PHARMACOLOGY
Class
Serotonin antagonist with anti-emetic properties
Action
Blocks the 5-HT3 receptors in the small intestines and the CTZ (Chemoreceptor trigger zone).
Metabolism
 Metabolised by the liver.
 Excreted in the faeces and urine.
 Drug or chemically induced nausea and vomiting.
 Acute vomiting following gastro-enteritis
 Obstetrics induced nausea and vomiting
Contraindications
Precautions
 Liver impairment
 Route of Administration
 IV / IM
Side Effects
Common:
 Headache
 Constipation
Rarely:
 Hypersensitivity reactions,
 Cardiovascular (tachycardia, hypotension, chest pain),
 Pain and redness around injection site.
Special Notes
 Onset rapid
 Peak: 1-2 hours
 Duration 3 hours
DOSAGE
ADULTS
 4mg IV /IM. IV dose must be diluted in 10-20ml of normal saline and given over 3-5
minutes.
PAEDIATRICS
 0.1mg/kg IV/IM up to a maximum of 4mg as per above.
PAEDIATRIC ONDANSETRON DOSAGES
Concentration: 4 mg/2 ml
Weight IV/IO/IM (0.1 mg/kg) Volume
3 kg 0.3 mg 0.15 ml
4 kg 0.4 mg 0.2 ml
5 kg 0.5 mg 0.25 ml
6 kg 0.6 mg 0.3 ml
7 kg 0.7 mg 0.35 ml
8 kg 0.8 mg 0.4 ml
9 kg 0.9 mg 0.45 ml
10 kg 1 mg 0.5 ml
12 kg 1.2 mg 0.6 ml
14 kg 1.4 mg 0.7 ml
16 kg 1.6 mg 0.8 ml
18 kg 1.8 mg 0.9 ml
25 kg 2.5 mg 1.25 ml
28 kg 2.8 mg 1.4 ml
31 kg 3.1 mg 1.55 ml
34 kg 3.4 mg 1.7 ml
37 kg 3.7 mg 1.85 ml
40 kg 4 mg 2 ml
43 kg 4 mg 2 ml
Paracetamol
PHARMACOLOGY
Class
Analgesic and anti-pyretic
Action
 A simple pain-killing medicine used to treat mild to moderate pain and fever.
 Reduces the production of prostaglandins in the brain and spinal cord – thus de-sensitising the
nerve endings to pain – thus increasing our pain threshold.
 Reduces fever through the area of the brain that regulates temperature (the hypothalamic
heat-regulating centre)
Metabolism
 Inactive metabolite excreted by the kidneys
 Treating mild to moderate pain
 Reducing fever (oral only)
 Obstetric pain
Contraindications
Known sensitivity or allergy to any ingredient
Precautions
 Use with caution in patients with decreased liver function.
 Use with caution in patients with decreased kidney function.
 Oral
 IV [AP and CCP for Adults; CCP only in Paediatrics]
Side Effects
 Skin rash
 Bradycardia if administered too quickly
Special Notes
 Safe in pregnancy
 Safe in breastfeeding
 Maximum of 8 tablets/ capsules in a 24-hour period
 IV solution
DOSAGE
ADULTS
PAIN AND FEVER
 500 - 1000mg orally (1-2 tablets)
MODERATE PAIN
 < 50kg: 15mg/kg IV slow infusion
 > 50kg 1000mg. Maximum adult dose 15mg/kg. Administer the infusion over
20 minutes.
PAEDIATRICS
MODERATE PAIN:
 15mg/kg IV and infants 7.5mg/kg. Maximum paediatric dose 20mg/kg. [CCP only]
FEVER:
 Oral solution dose: 15mg/ kg of a 120 mg/ 5ml (or 24mg/ ml)
Warnings:
 If the preparation is in a glass bottle. There is a risk of air embolism when the bottle
runs empty. Careful monitoring of the infursion is required.
 DO NOT REPEAT DOSAGE — Overdose will lead to liver damage and failure.
PAEDIATRIC PARACETAMOL DOSAGES
Weight IV/IO (7.5 mg/kg) Volume Oral (15 mg/kg) Volume

3 kg 22.5 mg 2.3 ml 45 mg 1.9 ml
4 kg 30 mg 3 ml 60 mg 2.5 ml
5 kg 37.5 mg 3.8 ml 75 mg 3.1 ml
6 kg 45 mg 4.5 ml 90 mg 3.8 ml
7 kg 52.5 mg 5.3 ml 105 mg 4.4 ml
8 kg 60 mg 6 ml 120 mg 5 ml
9 kg 67.5 mg 6.8 ml 135 mg 5.6 ml
10 kg 75 mg 7.5 ml 150 mg 6.3 ml
12 kg 180 mg 18 ml 180 mg 7.5 ml
14 kg 210 mg 21 ml 210 mg 8.8 ml
16 kg 240 mg 24 ml 240 mg 10 ml
18 kg 270 mg 27 ml 270 mg 11.3 ml
25 kg 375 mg 37.5 ml 375 mg 15.6 ml
28 kg 420 mg 42 ml 420 mg 17.5 ml
31 kg 465 mg 46.5 ml 465 mg 19.4 ml
34 kg 510 mg 51 ml 510 mg 21.3 ml
37 kg 555 mg 55.5 ml 555 mg 23.1 ml
40 kg 600 mg 60 ml 600 mg 25 ml
43 kg 645 mg 64.5 ml 645 mg 26.9 ml
Phenylephrine
PHARMACOLOGY
Class
Sympathomimetic
Action
Direct action on alpha-1 receptors causing vasoconstriction of arterioles.
Metabolism
Extensively metabolised in the liver primarily by monoamino oxidase deanimation

 Symptomatic hypotension following drug induced vasodilatation (RSI, sedation)
 Head injury with MAP < 90 mmHg AND sedation
 Septic Shock AND symptoms consistent with hypotension AFTER fluid resuscitation as per CPG
 Anaphylactic Shock in conjunction with and AFTER epinephrine as per CPG
 Neurogenic Shock AND symptoms due to hypotension
Contraindications
Hypersensitivity to components (metabisulfite, prevalence unknown but probably low, not clinically
relevant)
Precautions
 Dilute into 100 ml N/S or Dextrose 5% before use
 Monitor BP closely during use
 Use by syringe driver only except when immediate action is required while system is set up
 IV
 IO
Side Effects
 Reflex bradycardia (as a response to hypertension following administration)
 AV block
 Myocardial ischaemia
 NB: All of the above are as a result of relative overdose and short lived
Special Notes
 Onset rapid
 Peak 1 - 2 minutes
 Duration up to 20 minutes
DOSAGE
 START INFUSION AS SOON AS PRACTICAL:

 Add 10mg to 100ml Saline or 5% dextrose bag
 Draw up 50 ml of solution and infuse at 60 ml/h (100 mcg/min) initially and monitor BP
closely every 2 minutes.
 STOP infusion temporarily if BP > 190 mmHg systolic or sudden bradycardia
 Once BP starts to recovers reduce rate to 30 ml/h (50 mcg/min)
 The objective is to keep BP relatively constant
 Reduce by 2.5 - 5ml/h (4.15 - 8.3mcg/min) if BP remains elevated above desired level.
 Increase infusion by 5 ml/h (8.3 mcg/min) to 10 ml/h (16.6 mcg min) increments if BP be-
low desired level
 IF STARTING INFUSION IS NOT PRACTICAL OR IMMEDIATE ACTION IS
REQUIRED e.g. RSI:
 Give 0.5 ml – 1 ml (50 - 100 mcg) every 2-5 min, duration 10-20 min
Prochlorperazine (Stemetil)
PHARMACOLOGY
Class
Dopamine (D2) receptor antagonist with anti-emetic and anti-vertigo properties.
Action
 Dopamine antagonism has action directly on labyrinthine apparatus and on the CTZ (Chemore-
ceptor trigger zone).
 Weak antihistamine and anticholinergic effects.
 Potentiation of Noradrenaline
Metabolism
 Metabolised by the liver and excreted through bile and urine.
Primary Emergency Indications (Non-Emergency Service only)
 Nausea and vomiting due to motion sickness
 Vomiting from inner ear disorders (vertigo)
Contraindications
 Circulatory collapse
 CNS depressions (Coma or drug intoxication)
 Bone marrow depression
Precautions
 Should be avoided in patients with renal dysfunction, Parkinsons, hypothyroidism, phaeochromo-
cytoma, Myasthenia Gravis and Prostrate hypertrophy
 Use with care in the elderly and those potential for hypotension
 Epileptics – may precipitate seizures
 May prolong QT interval, use with caution in patients with arrhythmias.
 Use with caution in liver disease – due to primary hepatic metabolism.
 Hyperglycaemia: Diabetics should be closely monitored with use as it may cause a rise in blood
glucose levels.
Deep IM
Side Effects
 Drowsiness, akathisia, parkinsonism
 Constipation and dry mouth
 Blurred vision
 Hypotension, cardiac arrhythmias,
 Hyperglycaemia
 Urinary retention
 Seizures in epileptics, hyperpyrexia
Special Notes
 Onset: rapid
 Prochlorperazine can cause serious acute dystonic reactions in children leading to cyanosis from
laryngospasm, apnoea requiring ventilation, life threatening tetanus-like syndromes, coma or
even death. These reactions can occur from even a single therapeutic dose.
DOSAGES
 Adults only: 12.5mg deep IM
Rocuronium
PHARMACOLOGY
Class
 Non-depolarising neuromuscular paralytic (with fast onset and intermediate duration)
 “Curariform”
Action
 It competes with ACh at the post-synaptic ACh receptors, preventing the binding of Ach (competi-
tive antagonist)
 Produces total skeletal muscle paralysis without depolarisation or fasciculations
Metabolism
 Excreted in the urine and the bile
 Ongoing paralysis after RSI intubation
 When paralysis is required in the intubated patient, eg. post-ROSC
 Primary paralysis if a depolarising paralytic is contra-indicated or unavailable.
Contraindications
 Known hypersensitivity to Rocuronium or the Bromide ion or any of the excipients
 Known anaphylaxis to any neuromuscular blocking agent
 Personal or familial history of malignant hyperthermia
Precautions
 These precautions are mostly relevant to the hospital environment:
 Use with caution in patients with neuromuscular disease – eg. Myasthenia Gravis or
Lambert-Eaton syndrome – will cause profound paralysis
 Geriatric patients or those with clinically significant hepatic disease may experience a prolonged
duration of action (Consider 0.6 mg/kg dose)
 In hypothermia, the neuromuscular blocking effect of Rocuronium is increased and the duration
of action is prolonged.
 Patients with burns are known to develop resistance to non-depolarising neuromuscular blocking
agents. Titrate dose to response.
 Patients with severe electrolyte disturbances, altered blood pH or dehydration may experience
increased effects of Rocuronium.
 Rocuronium can have an increased effect after the administration of Suxamethonium
 IV
 IO
Side Effects
 Anaphylactic reactions (especially in patients who have had anaphylactic reactions to other types
of neuromuscular blocking agents)
 Prolonged neuromuscular blockade beyond the expected time – effects vary from skeletal muscle
paralysis to respiratory insufficiency or prolonged apnoea.
 Apnoea, bronchospasm and wheezing
 Arrhythmias including tachycardia
 Can induce an episode of malignant hyperthermia in susceptible individuals
Special Notes
 Must be administered with a sedative – Rocuronium has no effect on consciousness, pain thresh-
old or cerebration.
 Ability to adequately ventilate the patient must be established prior to the administration of Rocu-
ronium – due to its extended half life.
 It’s action is antagonised by acetylcholinesterase inhibitors such as Neostigmine, Edrophonium
and Pyridostigmine
 Should be stored in the refrigerator at 2-8ºC. Can be stored outside the refrigerator – up to 30ºC
for a period of 12 weeks.
 Peak 15 minutes
 Duration 30 minutes
DOSAGE
ADULT
RSI PRIMARY PARALYTIC AGENT
 Rocuronium 1 - 1.5mg/ kg
POST RSI PARALYSIS FOR VENTILATION

 Rocuronium 1mg/ kg as necessary. If using Rocuronium as the primary paralyzing
agent, further Rocuronium may not be immediately necessary.
 Dose may be repeated after 30 minutes if required
Salbutamol
PHARMACOLOGY
Class
Synthetic Beta-adrenergic stimulant – with primarily B2 effects
Action
By activating bronchial and vascular smooth muscle Beta-2 receptors it works to:
 Lungs = bronchodilation
 Vasculature = vasodilation
 Uterus = uterine relaxation
Metabolism
 Respiratory distress associated with bronchospasm
 Asthma
 COPD
 Severe allergic reactions
 Smoke inhalation
Contraindications
 Hypersensitivity to the drug or any ingredient in its composition.
 Patients with cardiac tachyarrhythmias
 Patients at risk of threatened abortion in the 1st or 2nd trimester (only as a tocolytic, not in the
presence of bronchoconstriction).
Precautions
Use with caution in patients with known heart disease.
 Nebulised
 IV – bolus and infusion
Side Effects
 Sinus tachycardia (usually secondary to a reduction in peripheral resistance due to vasodilation)
 Muscle tremor – secondary to Beta-2 stimulation in skeletal muscle.
 Palpitations
 Anaphylaxis
 Cardiac arrhythmias in susceptible patients
 Paradoxical bronchospasm (cease treatment immediately in this case)
Special Notes
 Patients in severe respiratory distress with minimal tidal volume may not benefit from nebulised
Salbutamol
 Patients with adequate tidal volume may not receive any benefit from IV salbutamol over inhaled
Salbutamol
 HR, BP and ECG should be continuously monitored with administration of Salbutamol
 Ventolin IV solution must not be administered undiluted – the concentration must be reduced
50% prior to administration.
 Oxygen should be continuously administered between nebulised doses of Salbultamol.
 Large doses of IV Salbutamol have been reported to cause intracellular metabolic acidosis.
 Patients on non-cardioselective Beta-blockers may have a reduced response to Salbutamol
 Nebulised Effects
 Intravenous Effects
DOSAGE
ADULT
RESPIRATORY DISTRESS WITH BRONCHOSPASM
 Salbutamol 5mg via nebuliser
 Repeat with 5mg if no initial response
 IV Salbutamol 250mcg over 10 minutes
Dilution:
 500mcg (i.e. 1 ampoule of 500mcg) with 49 mls 0.9% NaCl to 50ml in a 50 ml syringe
 Final concentration is 10 mcg/ml
 Dosage:
 Infuse 25mls over 10 minutes
 Syringe pump runs at 150mls/hr
PAEDIATRIC
RESPIRATORY DISTRESS ASSOCIATED WITH BRONCHOSPASM
 Salbutamol nebulised 2.5-5mg via nebulizer
 Repeat with 2.5-5mg if no initial response
 IV Salbutamol 10mcg/kg (maximum 250mcg) over 10 minutes
PAEDIATRIC SALBUTAMOL DOSAGE
Severe Asthma
IV/IO (10 mcg/kg over 10 min-
Weight Volume
utes)
Dilute: 500 mcg/1 ml + 49 ml NaCl = 500 mcg
/ 50 ml (or 10 mcg/ml)
3 kg 30 mcg 3 ml
4 kg 40 mcg 4 ml
5 kg 50 mcg 5 ml
6 kg 60 mcg 6 ml
7 kg 70 mcg 7 ml
8 kg 80 mcg 8 ml
9 kg 90 mcg 9 ml
10 kg 100 mcg 10 ml
12 kg 120 mcg 12 ml
14 kg 140 mcg 14 ml
16 kg 160 mcg 16 ml
18 kg 180 mcg 18 ml
>25kg 250 mcg 25 ml
Succinylcholine (suxamethonium)
PHARMACOLOGY
Class
 Depolarising neuromuscular blocking agent
 ACh receptor antagonist
Action
 Short acting muscle relaxant
 Mimics ACh as it binds with the cholinergic receptors on the motor end plate
 Produces total skeletal muscle paralysis with fasciculations
Metabolism
 Metabolised by pseudo-cholinesterase in the plasma
 Rapid sequence intubation (RSI)
Contraindications
 Known hypersensitivity to succinylcholine or any of its ingredients
 Major burns older than 24 hours
 Personal or familial history of malignant hyperthermia
 Electrolyte abnormalities – especially hyperkalaemia
 Penetrating eye injuries
 Skeletal muscle myopathies (eg. Duchenne muscular dystrophy)
 Denervation of skeletal muscle
Precautions
 Crush injuries
 Airway trauma
 If the patient has experienced an anaphylactic reaction to any neuromuscular blocking agent
(depolarising or non-depolarising).
 Patients on Digoxin – the risk of abnormal heart rhythms may be increased.
 Administration in the presence of organophosphate poisoning will cause prolonged paralysis and
should be avoided.
 IV
 IO
Side Effects
 Increased intraocular pressure
 Increased intragastric pressure
 Elevated serum potassium levels
 Malignant hyperthermia
Special Notes
 Sedation is required prior to administration
 A second dose of Suxamethonium usually causes profound bradycardia
 Refrigeration is required
 Onset 30-60 seconds
DOSAGE
ADULT
RSI
 150 mg for small adults (less than 60kgs estimated body weight)
 200mg for the average to large adult
Tranexamic Acid (TXA)
PHARMACOLOGY
Class
 Antifibrinolytic agent
 Synthetic derivative of amino acid (lysine)
Action
 TXA blocks formation of plasmin from plasminogen
 At high concentrations, TXA non-competitively inhibits plasmin
 Prevents clot breakdown, aiding in bleeding control
Metabolism
 Excreted renally (>95% as unchanged drug)
Primary Emergency indications

 Suspected Major Haemorrhage OR
 Major Haemorrhage with SBP < 90mmHg and/or HR > 110 beats/min
 Major Haemorrhage due to Ante-Partum or Post-Partum Haemorrhage
Contraindications
 Children under 14 years old
 Isolated head trauma
 Obvious resolution of haemorrhage
 Allergy to TXA
Precautions
 Do not administer TXA in the same IV line as blood
 Ensure clear handover to hospital Trauma team that TXA was administered
 Rapid bolus may cause hypotension
Route of administration
 IV
 IO
Side Effects
 Nausea, vomiting and diarrhoea
 Thromboembolic events (rare)
 Other rare side effects include disturbances in color vision, convulsions, allergic skin reactions
Special notes
 Clearly identify the patient who received TXA and notify hospital accordingly
 Initial TXA loading bolus dose requires a follow-up infusion at hospital
 Store below 30ºC
 Onset 5 - 15 minutes
 Duration 3 hours
DOSAGE
 1 gram (2 x 500mg ampoules) in 100ml NS run over 5-10 min.
 No repeat dose in pre-hospital environment – notify hospital staff so that the
follow-up infusion can be started in hospital.
Vecuronium
PHARMACOLOGY
Class
 Non-depolarising neuromuscular blocking agent (paralytic)
 Curariform
Action
 Moderate to long acting skeletal muscle relaxant
 Competes with Ach at post-synaptic Ach receptors – preventing the binding of Ach – acts as a
competitive antagonist
 Produces skeletal muscle paralysis without depolarisation or fasciculations
Metabolism
 Excreted in the urine and the bile
 Primary Emergency Indications
 Ongoing paralysis after RSI
 Ongoing paralysis after RSI intubation
 When paralysis is required in the intubated patient, eg. post-ROSC
 Primary paralysis if a depolarising paralytic is contra-indicated or unavailable.
Contraindications
Known hypersensitivity
Precautions
 Patients with Myasthenia Gravis or myasthenic (Eaton-Lambert) syndrome, small doses may
have profound effects. Reduced doses are suggested.
 Patients who have experienced anaphylactic reactions to any neuro-muscular blocking agent
(depolarising or non-depolarising) should be monitored carefully for an anaphylactic reaction to
Vecuronium.
 Consider using lower doses in patients with renal failure, as they may experience prolonged
effects of Vecuronium.
 Delayed onset of action may be experienced in patients with cardiovascular disease and slower
circulation time – do not increase the dose, give time for the drug to circulate adequately
 Consider using reduced doses in patients with cirrhosis or hepatic disease, as they may have
prolonged recovery times – due to the impaired metabolism.
 IV
 IO
Side Effects
 Extension of the drug’s pharmacological action beyond the time needed (most common side
effect)
 Anaphylactic reaction/ hypersensitivity reaction
 Muscle atrophy with long-term use
Special Notes
 Onset: approximately 1 minute
 Peak: approximately 3-5 minutes
 Duration: 45-60 minutes (95% complete recovery)
 Ensure the patient is adequately sedated during the duration of Vecuronium (as it is only a block-
ing agent and has no other properties)
 Ensure the patient can be ventilated prior to administration of Vecuronium.
 Will cause profound paralysis in patients with Myasthenia Gravis or Lambert-Eaton syndrome
 Prior administration of Suxamethonium may enhance the neuromuscular blocking effects and
duration of action of Vecuronium.
 Repeated administration of Vecuronium has little or no cumulative effect on the duration of neuro-
muscular blockade – therefore further doses can be administered with certainty of the duration of
effects
 Vecuronium is reversed with anticholinesterase agents, eg. Neostigmine
DOSAGE
 0.1mg/ kg IVI for paralysis post ETT/ LT insertion in RSI OR 0.3mg/ kg IVI for use as
a primary paralytic agent.
 Repeat at 30-minute intervals
RAPID SEQUENCE INDUCTION
QUICK REFERENCE GUIDE
Option 1: Rocuronium as primary paralyzing agent (Preferred)
UNSTABLE STABLE
S M L S M L
Fentanyl mcg (1 to 3mcg/kg) 50 75 100 150 200 300
Ketamine mg (1 to 2mg/ kg) 50 75 100 100 150 200
mg
Rocuronium 50 100 150 50 100 150
Option 2: Suxamethonium as primary paralyzing agent
UNSTABLE STABLE
S M L S M L
Fentanyl mcg (1 to 3mcg/kg)
50 75 100 150 200 300
Ketamine mg (1 to 2mg/ kg)
50 75 100 100 150 200
mg
Suxamethonium 200 200 200 200 200 200
Ongoing sedation and paralysis (as necessary) - ALL PATIENTS
S M L
Ketamine mg (0.5mg/ kg) 25 35 50
Fentanyl mcg (0.5mcg/kg) 25 35 50
Rocuronium mg (1mg/ kg)

50 100 150
st
At 30 min following 1 dose or as
necessary
Ideal Body Weight in kg = height (cm) minus 100

Round off drug doses to the nearest practical whole number
S = ⩲50-60kg; M = ⩲70-90kg; L = ≥100kg
Extended Pharmacopeia Retrieval Services
GENERIC DRUG NAME CONCENTRA-

TION
May be administered by a CCP follow-

METOPROLOL 1mg/ml VIAL
ing advice from SILVER CLINICAL

CEFTRIAXONE 1g VIAL

CISATRACURIUM 20mg/ 10ml VIAL

DEXAMETHASONE 8mg/ 2ml VIAL

DEXTROSE 50% 50%/ 50ml VIAL

DOBUTAMINE 250mg/ 20ml VIAL

DOXAPRAM 20mg/ 5ml VIAL
ENOXOPARIN May be administered by a CCP follow-

40mg VIAL
(CLEXANE) ing advice from SILVER CLINICAL

GLUCAGON 1G VIAL

HALOPERIDOL 5mg/ ml VIAL

HEPARIN 5000IU/ mlL VIAL

HYDRAZALINE 25mg VIAL

HYOSCINE 20mg/ ml VIAL

INSULIN REGULAR 100IU/ 10ml VIAL
GENERIC DRUG NAME CONCENTRA-
TION

KETOROLAC 30mg/ ml VIAL

LABETOLOL 100mg/ 20ml VIAL

LIGNOCAINE 1% 200mg/ 20ml VIAL

PHENYTOIN SODIUM 250mg/ 5ml VIAL

POTASSIUM CHLORIDE 20mmol/10ml VIAL

PROPOFOL 1% 20ml VIAL
SODIUM BICARBONATE PREFILLED May be administered by a CCP follow-

50ml SYRINGE
8.4% PFS ing advice from SILVER CLINICAL
MEDICATION PRIVILEGES
Medication Level 1 Level 2 Level 3 Level 4
Adenosine √
Adrenaline/Epinephrine √
Amiodarone √
Aspirin √ √ √ √
Atropine √
Budesonide √
Calcium Chloride √
Clopidogrel √ √ √
Dexamethasone √
Dextrose Oral √ √ √ √
Dextrose IV √ √
Diclofenac IM √ √ √
Diclofenac IV √ √
Diphenhydramine √
Fentanyl √
Furosemide √
Glucagon IM √ √ √
Glucagon IV √
Glycerol Trinitrate GTN (SL) √ √ √ √
Glycerol Trinitrate GTN (IV) √
Hydrocortisone √
Ibuprofen √ √ √ √
Ipratropium Bromide √ √ √
Ketamine √
Ketorolac (IM) √ √ √
Ketorolac (IV) √ √
Magnesium Sulphate √
Methoxyflurane (Penthrox) √ √ √ √
Metoclopramide √
Midazolam √
Naloxone √
Noradrenaline √
Ondansetron √
Paracetamol Oral √ √ √ √
Paracetamol IV √ √
Phenylephrine √
Prochlorperazine √
Rocuronium √
Salbutamol UDV √ √ √
Salbutamol IV √
Succinylcholine √
Tranexamic Acid (TXA) √
Vecuronium √
Level 2 privileged practitioners may continue and monitor
previously prescribed Level 3 IV/IM medications
Acknowledgements
Thank you to the following people who played a significant part in the development and review of the
2019 edition of the HMCAS Clinical Practice Guidelines.
Contributors:
Dr. Nicholas Castle

Mr Ian Howland
Mr. Yugan Pillay
Mr. Ian Howard
Mrs. Beverley Ludick
Dr. Padarath Gangaram
Mrs. Kirsten Uhde
Design:
Ma. Karbee Alvendia
Mr. Joel Sayo
Mr. Roumel Ramos
HMCAS CLINICAL PRACTICE GUIDELINES Version 1.4 2019 PAGE 347


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Ambulance Service

Clinical Practice Guidelines

CPG Ver. 1.4. - 2019

1.0 Initial Draft Mr. Casey Walker 2016

1.1 Addendum CW, JPS 20170509

1.1 final addendum and corrections CW, JPS 20170805

1.2 version no. updated JPS 20170809

1.3 Quarterly update (changes IRH, YP, ILH, BDL, NC 20180517

Dr. Loua Al Sheik, Medical Director

Dr. Robert Owen, CEO HMCAS

Mr. Brendon Morris, Executive Director

Dr. Nicholas Castle, Head of Profession

Dr. Padarath Gangaram, A/SOM:

H.E. Hanan Al-Kuwari PhD

Dr. Loua Asad Hanna Al Shaikh

The purpose of these HMCAS Clinical Practice Guidelines are to:

 Saving and preserving of life

Dr. Nicholas Castle

PROCEDURE AP CCP COMMENTS

ADULT MEDICAL GUIDELINES

CPG 3.1 Management of Adult Acute Bronchoconstriction

CPG 4.1 Adult Medical Cardiac Arrest Management 53

CPG 5.1 Management of Stroke 77

CPG 6.1 Management of Pain 83

CPG 7 Management of Hyperglycaemia and Hypoglycaemia 93

CPG 8 Management of Drug Overdose and Poisoning 94

ADULT TRAUMA GUIDELINES

CPG 11 Management of Combative Patient 135

INTER-FACILITY TRANSFER GUIDELINES

Rapid Sequence Induction Quick Reference Guide 343

Extended Pharmacopeia Retrieval Services 344

Medication Privileges 346

CPG 2.1 ADULT FOREIGN BODY AIRWAY OBSTRUCTION 14

Dextrose (oral & IV) 272

Glycerol Trinitrate - GTN (sublingual and IV) 287

Magnesium sulphate 304

ACS Acute Coronary Syndrome ETT Endo Tracheal Tube(s)

A-P Anteroposterior gm Gram

APH Antepartum Haemorrhage Hb, Hgb Hemoglobin

ARF Acute Renal Failure h/o History of

AVPU Alert, Verbal, Painful, Unresponsive HR Heart Rate

mV Millivolt RBS Random Blood Sugar

NaCl Sodium Chloride RSI Rapid Sequence Induction

NSR Normal Sinus Rhythm SIMV

NSAID Non-steriod Anti-Inflammatory Drug SL Sublingual (Under the Tongue)

PAF Paroxysmal Atrial Fibrillation T Temperature

Pupils Equal, Round, Reactive to Light UTI Urinary Tract Infection

PID Pelvic Inflammatory Disease Vtach Ventricular Tachycardia

PND Paroxysmal Nocturnal Dyspnea x/7 number of days

dc could mean “discontinue” or “discharge” discontinue or discharge

CLINICAL APPROACH TO AN ADULT

The adult patient is defined as a person of 14 years or older.

The vital sign monitoring requirements in this guideline

Consent should be obtained prior to performing any

TABLE 1. NORMAL VITAL SIGN RANGE FOR ADULT PATIENTS

VITAL SIGN NORMAL RANGE

RESPONDER SAFETY AND SCENE SIZE-UP

ABC life threats must be treated as soon as they are

3. Confirm the Chief Complaint

HMCAS QEWS TABLE

Initiate immediate life support therapy as required:

The situation report to NCC should include the following:

HMCAS CLINICAL PRACTICE GUIDELINES Version 1.4 2019 CPG 1 PAGE 4